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The week at Retraction Watch featured:

• How a now-retracted study got published in the first place, leading to a $3.8 million NIH grant
• Did a nasty publishing scheme help an Indian dental school win high rankings?
• Flagrant and frankly, inexcusable data duplication leads to retraction
• Journal pulls paper from Ethiopia for unlicensed use of questionnaire

Our list of retracted or withdrawn COVID-19 papers is up to more than 300. There are now 40,000 retractions in our database  which powers retraction alerts in EndNote, LibKey, Papers, and ...

In 2021, the American Psychiatric Association (APA), the guild of U.S. psychiatrists, acknowledged its history of racism. However, it is difficult to imagine how psychiatry will ever acknowledge that its entire edifice is built on a fundamental bigotry.

Bigotry is defined by Merriam-Webster as: obstinate or intolerant devotion to ones own opinions and prejudices. Racism is one type of bigotry, but not the only type. The fuel of all bigots is the same: the belief that their discomfort over others different from themselves justifies declarations of defectiveness in others.

While discomfort over racial differences fuels racial bigotry, the discomfort over other human differences fuels psychiatrys opinions and prejudices with respect to all its diagnostic declarations as to which behaviors evidence mental illness and which are normal. All bigots reduce their discomfort by declaring others different from themselves as defective in some manner.

The APAs Political Apology for Structural Racism

Just as it has been long known to Black Americans that being Black makes them more vulnerable to police violence, being Black also makes one more vulnerable to psychiatric violence.

Why, in 2021, did the APA finally issue the APAs Apology to Black, Indigenous and People of Color for Its Support of Structural Racism in Psychiatry (followed by its Historical Addendum to APAs Apology to Black, Indigenous and People of Color for Its Support of Structural Racism in Psychiatry)? The APA makes clear what precipitated their apology: Events in 2020 have clearly highlighted the need for action by the APA to reverse the persistent tone of privilege built upon the inhumanity of past events.

While the APA has a long history of ignoring science and perpetuating social injustices, it has just as long a history of attempting to be politically in step with mainstream U.S. society. Following the 2020 murder of George Floyd by police, the APA recognized that the U.S. political climate had dramatically changed. In this new climate, not only would there be no political cost for the APA to acknowledge psychiatrys racism, the APA recognized that it may well be a political win for them to proclaim their historical racism as loudly as possible. The APA recognized that in this new climate, to acknowledge racism is evidence of virtue, so virtue signaling the APA did. The politically astute APA knows that in todays political climate, institutions will not lose status for acknowledging......

PMID:  Int J Mol Sci. 2023 Jan 11 ;24(2). Epub 2023 Jan 11. PMID: 36674937 Abstract Title:  Polysaccharide Ameliorated Antibiotic-Associated Diarrhea in Mice via Regulating the Homeostasis of the Gut Microbiota and Intestinal Mucosal Barrier. Abstract:  polysaccharides (PCP) have been validated for several biological activities, including antitumor, anti-inflammatory, antioxidant, immunomodulatory, hepatoprotective and modulation on gut microbiota. In this research, we aim to demonstrate the potential prebiotic effects and the therapeutic efficacies of PCP in the treatment of antibiotic-associated diarrhea (AAD), and confirm the beneficial effects of PCP on gut dysbiosis. Antibiotic-associated diarrhea mice models were established by treating them with broad-spectrum antibiotics in drinking water for seven days. Mice in two groups treated with probiotics and polysaccharide were given Bifico capsules (4.2 g/kg/d) and PCP (250 mg/kg/d) for seven days using intragastric gavage, respectively. To observe the regulatory effects of PCP on gut microbiota and intestinal mucosal barrier, we conducted the following experiments: intestinal flora analysis (16S rDNA sequencing), histology (H&E staining) and tight junction proteins (immunofluorescence staining). The levels of mRNA expression of receptors associated with inflammation and gut metabolism were assessed by real-time reverse transcription-polymerase chain reaction (RT-PCR). The study revealed that PCP can comprehensively improve the clinical symptoms of AAD mice, including fecal traits, mental state, hair quality, etc., similar to the effect of probiotics. Based on histology observation, PCP significantly improved the substantial structure of the intestine of AAD mice by increasing the expression levels of colonic tight junction protein zonula-occludens 1 (ZO-1) and its mRNA. Moreover, PCP not only increased the abundance of gut microbiota, but also increased the diversity of gut microbiota in AAD mice, including alpha diversity and beta diversity. Further analysis found that PCP can modulate seven characteristic species of intestinal flora in AAD mice, including,,,,,andFinally, enrichment analysis predicted that PCP may affect intestinal mucosal barrier function, host immune response and metabolic function by regulating the microbiota. RT-PCR experiments showed that PCP can participate in immunomodulatory and modulation on metabolic by regulating the mRNA expression of forkhead-box protein 3 (FOXP3) and G protein-coupled receptor 41 (GPR41). These results indicated thatpolysaccharide may ameliorate antibiotic-associated diarrhea in mice by regulating the homeostasis of the gut microbiota and intestinal mucosal barrier. In addition, polysaccharide-derived changes in intestinal microbiota were involved in the immunomodulatory activities...

PMID:  Front Nutr. 2023 ;10:1119583. Epub 2023 Mar 27. PMID: 37051119 Abstract Title:  Characteristics and properties of a polysaccharide isolated fromas potential dietary supplement for IBS. Abstract:  INTRODUCTION: As low FODMAP (Fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet therapy is recommended for most of Irritable Bowel Syndrome (IBS) patients, the consequent insufficient of dietary fibers (DFs) intake exert an adverse impact on intestinal health. It is necessary to find suitable DFs for IBS patients.METHODS: This study extracted a water-insoluble polysaccharide from(WIP) by alkali-extraction and acid-precipitation method. Its molecular weight was detected by high performance gel permeation chromatography (HPGPC) analysis. The structure of WIP was analyzed by Fourier transform infrared (FT-IR) spectrum, Nuclear Magnetic Resonance (NMR) spectra and X-ray diffraction (XRD). The properties related to stability, digestion, viscosity, osmotic activity, adsorption and fermentation were investigated, aimed to explore the feasibility of WIP as a new DF supplement for patients with IBS. In addition, 16S rRNA sequencing analysis was conducted to explore its effects on IBS-related gut microbiota.RESULTS AND DISCUSSION: The results showed that WIP had a single homogeneous composition and the molecular weight was 8.110Da. WIP was indicated as a kind of pyranose form withanomeric configuration and the main chain of WIP was 1,3--glucan with amorphous structure. In addition to good thermal stability, WIP also has low bioavailability and can reach the colon mostly without being digested. Moreover, the low viscosity and osmotic activity, the high water- swelling and water/oil-holding capacity, fructose adsorption capacity and poor fermentation performance of WIP demonstrated that it is suitable for IBS patients. It is worth noting that WIP regulates IBS associated gut microbiota effectively, such as the abundance of Lachnospiraceae and Prevotella. These findings provide a theoretical basis for the development of WIP as a dietary supplement for IBS patients with low FODMAP diet therapy. GRAPHICAL ABSTRACT.

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PMID:  Life (Basel). 2023 Mar 27 ;13(4). Epub 2023 Mar 27. PMID: 37109422 Abstract Title:  Bioactive Compounds and Signaling Pathways ofin Suppressing Inflammatory Response by Network Pharmacology. Abstract:  (WE) is a medicinal mushroom and an excellent source of naturally occurring anti-inflammatory substances. However, the particular bioactive compound(s) and mechanism(s) of action against inflammation have yet to be determined. Here, we studied anti-inflammatory bioactive compounds and their molecular mechanisms through network pharmacology. Methanol (ME) extract of WE (MEWE) was used for GC-MS analysis to identify the bioactives, which were screened by following Lipinski's rules. Public databases were used to extract selected bioactives and inflammation-related targets, and Venn diagrams exposed the common targets. Then, STRING and Cytoscape tools were used to construct protein-protein (PPI) network and mushroom-bioactives-target (M-C-T) networks. Gene Ontology and KEGG pathway analysis were performed by accessing the DAVID database and molecular docking was conducted to validate the findings. The chemical reactivity of key compounds and standard drugs was explored by the computational quantum mechanical modelling method (DFT study). Results from GC-MS revealed 27 bioactives, and all obeyed Lipinski's rules. The public databases uncovered 284 compound-related targets and 7283 inflammation targets. A Venn diagram pointed to 42 common targets which were manifested in the PPI and M-C-T networks. KEGG analysis pointed to the HIF-1 signaling pathway and, hence, the suggested strategy for preventing the onset of inflammatory response was inhibition of downstream NFKB, MAPK, mTOR, and PI3K-Akt signaling cascades. Molecular docking revealed the strongest binding affinity for "N-(3-chlorophenyl) naphthyl carboxamide" on five target proteins associated with the HIF-1 signaling pathway. Compared to the standard drug utilized in the DFT (Density Functional Theory) analysis, the proposed bioactive showed a good electron donor component and a reduced chemical hardness energy. Our research pinpoints the therapeutic efficiency of MEWE and this work suggests a key bioactive compound and its action mechanism against inflammation.

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PMID:  Food Sci Nutr. 2023 May ;11(5):2356-2371. Epub 2023 Mar 9. PMID: 37181308 Abstract Title:  Effects ofextract and protein powder mixture on glucolipid metabolism and rhythm changes in obese mice. Abstract:  Herein, we explored the effects ofextract, protein powder mixture, and their combined intervention on weight loss in high-fat diet (HFD)-induced obese mice. Male C57BL/6J mice were selected and fed a HFD for 8weeks; obese mice that were successfully modeled were divided into modeling and five intervention groups, and given the corresponding treatment for 10weeks. Body weight, fat, and muscle tissue, blood glucose, lipids, inflammatory factors, and other glucose and lipid metabolism-related indicators were measured to evaluate the effect of. and protein powder intervention on weight loss in obese mice. The body weight of the intervention group was reduced compared with the HFD group. Fat content of mice in F3PM group decreased significantly ( 

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More Than a Billion People Have Seen Plandemic

Mikki Willis documentary, Plandemic Part 1 was released May 4, 2020, and has since been viewed over 1 billion times, a record, for sure, for any documentary. This, despite it being heavily censored. Plandemic Part 2: Indoctornation has been viewed more than 200 million times.

One of the keys to the videos remarkable successes was Willis decision to allow (and encourage) people to download the movie files and upload them anywhere they pleased, without restrictions.

This virtually guaranteed he wouldnt make any money from the films, but he viewed them as a gift to humanity. Putting the truth out there was more important than making a buck. Besides, hosting the films on any given platform would allow the opposition to simply nuke that one site, ensuring the films wouldnt be seen by anyone.

Plandemic 3 Will Expose Power Players and Their Intentions

Plandemic: Indoctornation features the brilliant David Martin, Ph.D., who has documented and tracked white collar crime for decades and invented technologies that help trace the flow of funding. Willis explains:

We decided in Plandemic 2 to really follow the paper trail. And I'm very glad we made that decision because it has been bulletproof. Every single claim that David Martin made in the film has been 100% validated at this point.

He's the one that actually helped educate [Sens.] Rand Paul and Ron Johnson when they started to go after [Dr. Anthony] Fauci to finally hold him accountable for his decades of crimes.

[Martin] had the paper trail of how much money had been spent, that had been moved through a company called EcoHealth Alliance, and where it ended up in Wuhan at the lab.

But as important as it is to know where the virus originated, it goes so far beyond that in the next [film]. We are, I will announce right now, producing Plandemic 3. And that one's going to go even further into who's behind this [virus] and why. Is this really about money? The answer is, for the most part, no. The people at the top of the pyramid, they can just print their own money.

It's really about ultimately creating a state of dependency, through which you can then control the human population. We're going to go deeper and really show the trail on how that works, the history of that, and how it's led us to this moment right now.

deal of our population into fighting for these very wicked forces, unknowingly, unwittingly.

After the release of Plandemic 1,...

Introduction

The pharmaceutical business model requires pharmaceuticals that are "effective" enough to somehow justify pushing them on patients but not effective enough to actually fix the issue the drug is prescribed for, thus requiring each patient to take the drug indefinitely. Furthermore, the larger the potential drug market is, the more aggressively the pharmaceutical industry will push to promote it to every available customer.

In some cases, such as for the dangerous and ineffective COVID-19 vaccines, this greed is so blatant even the general public can see it. Conversely, in other cases, it is typically invisible to any besides those directly affected by the drugs and their immediate family.

Recently, for example, I reviewed the statin catastrophe after Aseem Malhotra on the Joe Rogan show brought the public's attention to the danger and ineffectiveness of these drugs and how the same reprehensible forces we saw push the COVID-19 vaccines have been operating for decades within the cholesterol industry.

Although it's challenging to claim any one class of drugs is the "worst," a good case can be made for psychiatric medications. In addition to the drugs being dangerously addictive and most of their "benefits" coming from doctored research data, they have some disturbing side effects.

Beyond already tragic complications like fatal heart attacks (which happened to a close friend of mine), individuals on these drugs can become partially psychotic, and there are many tragic cases of suicides and homicides following their use.

Unfortunately, because of just how large this market is, the industry and the FDA have gone to extreme lengths to cover up the harms of these drugs for decades, and business as usual continues in the psychiatric sector.

Note: Much of this is difficult to believe, so I chronicled exactly what can now be proven happened with the antidepressants. I did this because what the FDA did back then is one of the closest precedents we have for understanding how the COVID-19 vaccines were handled and what to expect will happen in the future.

After I published an article summarizing the evidence for the psychotic, violent, and often deadly behaviors these drugs caused, Kim Witczak reached out to me to share her story. Soon after Zoloft entered the market, Kim's husband Woody was unnecessarily put on the drug and, not long after, suddenly killed himself in a manner characteristic of a Zoloft suicide.

Kim decided the best thing she could do with this tragic situat...

Editor's Note: This article is a reprint. It was originally published March 18, 2018.

Dr. Dan Engle, board-certified in adult psychology and neurology, and who completed psychiatric fellowships in child, adolescent and forensic psychiatry, has written an indispensable guide to recovering from traumatic brain injury (TBI), "The Concussion Repair Manual: A Practical Guide to Recovering From Traumatic Brain Injuries."

TBI is incredibly pervasive. An estimated 80% to 90% of people have had some form of TBI. Military personnel and athletes such as football players and boxers tend to be at particularly high risk, but TBI can happen to anyone, for a range of reasons. Engle has had personal experience with it, which is what motivated him to pursue this discipline of medicine and write a book about it.

"I went to college to play soccer Boxers who get slugged in the face that's about 20 pounds of pressure to their brain. Soccer players, if you go in for a full volley or a full header, take 70 pounds of pressure to the brain I had a series of concussions that led up to me choosing medical school," he says.

"Two weeks before medical school, I broke my neck. That was a big entry point in a recalibration of my direction I started [medical school] in a Halo Device, where they screw it into your skull and you're walking around fixated.

For the first three months of med school, I was in this Halo. It was the first thing that finally slowed me down. It helped me self-reflect. It helped me realize that I was driving at a level of intensity in my life that I didn't really enjoy.

I ended up having much more fun in med school and residency than I did in high school and college, just because I wasn't so intense with everything. It oriented me from ER and surgical medicine into neurology and psychiatry.

[My focus] was the neuroreparative aspects of brain injury and spinal cord injury, as well as the more humanistic side of understanding people, the stories of what make us who we are and the mindset of healing, and how very [important] that is to recovery."

TBIs Are Pervasive, yet Many Don't Get Proper Rehabilitation

A common myth is that unless you've suffered complete loss of consciousness, you didn't have a concussion or significant head injury, but this simply isn't true, Engle says. Generally speaking, a concussion is a mild TBI, and will score higher on assessment using the Glasgow Coma Scale (a scoring system that grades your level of consc...

PMID:  AMB Express. 2023 Mar 10 ;13(1):29. Epub 2023 Mar 10. PMID: 36897423 Abstract Title:  A fabricated hydrogel of hyaluronic acid/curcumin shows super-activity to heal the bacterial infected wound. Abstract:  High risk of acute morbidities and even mortality from expanding the antibiotics resistant infectious wounds force indefinite efforts for development of high performance wound-healing materials. Herein, we design a procedure to fabricate a hyaluronic acid (HA)-based hydrogel to conjugate curcumin (Gel-H.P.Cur). The highlight of this work is to provide a favorite condition for capturing curcumin while protecting its structure and intensifying its activities because of the synchronization with HA. Accordingly, HA as a major component of dermis with a critical role in establishing skin health, could fortify the wound healing property as well as antibacterial activity of the hydrogel. Gel-H.P.Cur showed antibacterial properties against Pseudomonas aeruginosa (P. aeruginosa), which were examined by bactericidal efficiency, disk diffusion, anti-biofilm, and pyocyanin production assays. The effects of Gel-H.P.Cur on the inhibition of quorum sensing (QS) regulatory genes that contribute to expanding bacteria in the injured place was also significant. In addition, Gel-H.P.Cur showed high potential to heal the cutaneous wounds on the mouse excisional wound model with repairing histopathological damages rapidly and without scar. Taken together, the results strongly support Gel-H.P.Cur as a multipotent biomaterial for medical applications regarding the treatment of chronic, infected, and dehiscent wounds.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):173-182. Epub 2022 Oct 6. PMID: 36926617 Abstract Title:  The ways for ginsenoside Rh2 to fight against cancer: the molecular evidencesand. Abstract:  Cancer is a global public health issue that becomes the second primary cause of death globally. Considering the side effects of radio- or chemo-therapy, natural phytochemicals are promising alternatives for therapeutic interventions to alleviate the side effects and complications. Ginsenoside Rh2 (GRh2) is the main phytochemical extracted from Panax ginseng C.A. Meyer with anticancer activity. GRh2 could induce apoptosis and autophagy of cancer cells and inhibit proliferation, metastasis, invasion, and angiogenesisand. In addition, GRh2 could be used as an adjuvant to chemotherapeutics to enhance the anticancer effect and reverse the adverse effects. Here we summarized the understanding of the molecular mechanisms underlying the anticancer effects of GRh2 and proposed future directions to promote the development and application of GRh2.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):274-282. Epub 2022 Sep 3. PMID: 36926615 Abstract Title:  Ginsenoside compound K reduces ischemia/reperfusion-induced neuronal apoptosis by inhibiting PTP1B-mediated IRS1 tyrosine dephosphorylation. Abstract:  BACKGROUND: Ginsenoside compound K (CK) stimulated activation of the PI3K-Akt signaling is one of the major mechanisms in promoting cell survival after stroke. However, the underlying mediators remain poorly understood. This study aimed to explore the docking protein of ginsenoside CK mediating the neuroprotective effects.MATERIALS AND METHODS: Molecular docking, surface plasmon resonance, and cellular thermal shift assay were performed to explore ginsenoside CK interacting proteins. Neuroscreen-1 cells and middle cerebral artery occlusion (MCAO) model in rats were utilized asandmodels.RESULTS: Ginsenoside CK interacted with recombinant human PTP1B protein and impaired its tyrosine phosphatase activity. Pathway and process enrichment analysis confirmed the involvement of PTP1B and its interacting proteins in PI3K-Akt signaling pathway. PTP1B overexpression reduced the tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) after oxygen-glucose deprivation/reoxygenation (OGD/R) in neuroscreen-1 cells. These regulations were confirmed in the ipsilateral ischemic hemisphere of the rat brains after MCAO/R. Ginsenoside CK treatment reversed these alterations and attenuated neuronal apoptosis.CONCLUSION: Ginsenoside CK binds to PTP1B with a high affinity and inhibits PTP1B-mediated IRS1 tyrosine dephosphorylation. This novel mechanism helps explain the role of ginsenoside CK in activating the neuronal protective PI3K-Akt signaling pathway after ischemia-reperfusion injury.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):210-217. Epub 2021 Apr 22. PMID: 36926614 Abstract Title:  Longevity, tumor, and physical vitality in rats consuming ginsenoside Rg1. Abstract:  BACKGROUND: Effects of the major ginsenoside Rg1 on mammalian longevity and physical vitality are rarely reported.PURPOSE: To examine longevity, tumor, and spontaneous locomotor activity in rats consuming Rg1.METHODS: A total of 138 Wistar rats were randomized into 2 groups: control (N = 69) and Rg1 (N = 69). Rg1 (0.1 mg/kg per day) were orally supplemented from 6 months of age until natural death. Spontaneous mobility was measured by video-tracking together with body composition (dual energy x-ray absorptiometry) and inflammation markers at 5, 14, 21, and 28 months of age.RESULTS: No significant differences in longevity (control: 706 days; Rg1: 651 days, = 0.77) and tumor incidence (control: 19%; Rg1: 12%, = 0.24) were observed between the two groups. Movement distance in the control group declined significantly by60% at 21 months of age, together with decreased TNF-( = 0.01) and increased IL-10 ( = 0.02). However, the movement distance in the Rg1 group was maintained50% above the control groups ( = 0.01) at 21 months of age with greater magnitudes of TNF-decreases and IL-10 increases. Glucose, insulin, and body composition (bone, muscle and fat percentages) were similar for both groups during the entire observation period.CONCLUSION: The results of the study suggest a delay age-dependent decline in physical vitality during late life by lifelong Rg1 consumption. This improvement is associated with inflammatory modulation. Significant effects of Rg1 on longevity and tumorigenesis were not observed.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):237-245. Epub 2022 Aug 6. PMID: 36926610 Abstract Title:  Protective effect and mechanism of ginsenoside Rg2 on atherosclerosis. Abstract:  BACKGROUND: Ginsenoside Rg2 (Rg2) has a variety of pharmacological activities and provides benefits during inflammation, cancer, and other diseases. However, there are no reports about the relationship between Rg2 and atherosclerosis.METHODS: We used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) to detect the cell viability of Rg2 in vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs). The expression of inflammatory factors in HUVECs and the expression of phenotypic transformation-related marker in VSMCs were detected at mRNA levels. Western blot method was used to detect the expression of inflammation pathways and the expression of phenotypic transformation at the protein levels. The rat carotid balloon injury model was performed to explore the effect of Rg2 on inflammation and phenotypic transformation.RESULTS: Rg2 decreased the expression of inflammatory factors induced by lipopolysaccharide in HUVECs-without affecting cell viability. These events depend on the blocking regulation of NF-B and p-ERK signaling pathway. In VSMCs, Rg2 can inhibit the proliferation, migration, and phenotypic transformation of VSMCs induced by platelet derived growth factor-BB (PDGF-BB)-which may contribute to its anti-atherosclerotic role. In rats with carotid balloon injury, Rg2 can reduce intimal proliferation after injury, regulate the inflammatory pathway to reduce inflammatory response, and also suppress the phenotypic transformation of VSMCs.CONCLUSION: These results suggest that Rg2 can exert its anti-atherosclerotic effect at the cellular level and animal level, which provides a more sufficient basis for ginseng as a functional dietary regulator.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):319-328. Epub 2022 Oct 5. PMID: 36926609 Abstract Title:  Korean Red Ginseng and Rb1 facilitate remyelination after cuprizone diet-induced demyelination. Abstract:  BACKGROUND: Demyelination has been observed in neurological disorders, motivating researchers to search for components for enhancing remyelination. Previously we found that Rb1, a major ginsenoside in Korean Red Ginseng (KRG), enhances myelin formation. However, it has not been studied whether Rb1 or KRG function in remyelination after demyelination.METHODS: Mice were fed 0.2% cuprizone-containing chow for 5 weeks and returned to normal chow with daily oral injection of vehicle, KRG, or Rb1 for 3 weeks. Brain sections were stained with luxol fast blue (LFB) staining or immunohistochemistry. Primary oligodendrocyte or astrocyte cultures were subject to normal or stress condition with KRG or Rb1 treatment to measure gene expressions of myelin, endoplasmic reticulum (ER) stress, antioxidants and leukemia inhibitory factor (LIF).RESULTS: Compared to the vehicle, KRG or Rb1 increased myelin levels at week 6.5 but not 8, when measured by the LFBor GST-piarea within the corpus callosum. The levels of oligodendrocyte precursor cells, astrocytes, and microglia were high at week 5, and reduced afterwards but not changed by KRG or Rb1. In primary oligodendrocyte cultures, KRG or Rb1 increased expression of myelin genes, ER stress markers, and antioxidants. Interestingly, under cuprizone treatment, elevated ER stress markers were counteracted by KRG or Rb1. Under rotenone treatment, reduced myelin gene expressions were recovered by Rb1. In primary astrocyte cultures, KRG or Rb1 decreased LIF expression.CONCLUSION: KRG and Rb1 may improve myelin regeneration during the remyelination phase, potentially by directly promoting myelin gene expression.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):337-346. Epub 2022 Nov 11. PMID: 36926607 Abstract Title:  Ginsenoside Rb2 suppresses cellular senescence of human dermal fibroblasts by inducing autophagy. Abstract:  BACKGROUND: Ginsenoside Rb2, a major active component of, has various physiological activities, including anticancer and anti-inflammatory effects. However, the mechanisms underlying the rejuvenation effect of Rb2 in human skin cells have not been elucidated.METHODS: We performed a senescence-associated-galactosidase staining assay to confirm cellular senescence in human dermal fibroblasts (HDFs). The regulatory effects of Rb2 on autophagy were evaluated by analyzing the expression of autophagy marker proteins, such as microtubule-associated protein 1A/1B-light chain (LC) 3 and p62, using immunoblotting. Autophagosome and autolysosome formation was monitored using transmission electron microscopy. Autophagic flux was analyzed using tandem-labeled GFP-RFP-LC3, and lysosomal function was assessed with Lysotracker. We performed RNA sequencing to identify potential target genes related to HDF rejuvenation mediated by Rb2. To verify the functions of the target genes, we silenced them using shRNAs.RESULTS: Rb2 decreased-galactosidase activity and altered the expression of cell cycle regulatory proteins in senescent HDFs. Rb2 markedly Moreover, Rb2 increased lysosomal function and red puncta in tandem-labeled GFP-RFP-LC3, which indicate that Rb2 promoted autophagic flux. RNA sequencing data showed that the expression of DNA damage-regulated autophagy modulator 2 (DRAM2) was induced by Rb2. In autophagy signaling, Rb2 activated the AMPK-ULK1 pathway and inactivated mTOR.knockdown inhibited autophagy and Rb2-restored cellular senescence.CONCLUSION: Rb2 reverses cellular senescence by activating autophagy via the AMPK-mTOR pathway and induction of DRAM2, suggesting that Rb2 might have potential value as an antiaging agent.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):183-192. Epub 2022 Nov 17. PMID: 36926608 Abstract Title:  Antiviral Potential of the Genus: An updated review on their effects and underlying mechanism of action. Abstract:  Viral infections are known as one of the major factors causing death. Ginseng is a medicinal plant that demonstrated a wide range of antiviral potential, and saponins are the major bioactive ingredients in the genuswith vast therapeutic potential. Studies focusing on the antiviral activity of the genusplant-derived agents (extracts and saponins) and their mechanisms were identified and summarized, including contributions mainly from January 2016 until January 2022.,, andwere included in the review as valuable medicinal herbs against infections with 14 types of viruses. Reports from 9 extracts and 12 bioactive saponins were included, with 6 types of protopanaxadiol (PPD) ginsenosides and 6 types of protopanaxatriol (PPT) ginsenosides. The mechanisms mainly involved the inhibition of viral attachment and replication, the modulation of immune response by regulating signaling pathways, including the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, cystathionine-lyase (CSE)/hydrogen sulfide (HS) pathway, phosphoinositide-dependent kinase-1 (PDK1)/ protein kinase B (Akt) signaling pathway, c-Jun N-terminal kinase (JNK)/activator protein-1 (AP-1) pathway, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) pathway. This review includes detailed information about the mentioned antiviral effects of the genusextracts and saponinsand, and in human clinical trials, which provides a scientific basis for ginseng as an adjunctive therapeutic drug or nutraceutical.

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n/a PMID:  J Ginseng Res. 2023 Mar ;47(2):255-264. Epub 2022 Aug 19. PMID: 36926604 Abstract Title:  Effect of fermented red ginseng on gut microbiota dysbiosis- or immobilization stress-induced anxiety, depression, and colitis in mice. Abstract:  BACKGROUND: Red ginseng (RG) alleviates psychiatric disorders. Fermented red ginseng (fRG) alleviates stress-induced gut inflammation. Gut dysbiosis causes psychiatric disorders with gut inflammation. To understand the gut microbiota-mediated action mechanism of RG and fRG against anxiety/depression (AD), we investigated the effects of RG, fRG, ginsenoside Rd, and 20(S)--D-glucopyranosyl protopanaxadiol (CK) on gut microbiota dysbiosis-induced AD and colitis in mice. METHODS: Mice with AD and colitis were prepared by exposing to immobilization stress (IS) or transplanting the feces of patients with ulcerative colitis and depression (UCDF). AD-like behaviors were measured in the elevated plus maze, light/dark transition, forced swimming, and tail suspension tests. RESULTS: Oral gavage of UCDF increased AD-like behaviors and induced neuroinflammation, gastrointestinal inflammation, and gut microbiota fluctuation in mice. Oral administration of fRG or RG treatment reduced UCDF-induced AD-like behaviors, hippocampal and hypothalamic IL-6 expression, and blood corticosterone level, whereas UCDF-suppressed hippocampal BDNFNeuNcell population and dopamine and hypothalamic serotonin levels increased. Furthermore, their treatments suppressed UCDF-induced colonic inflammation and partially restored UCDF-induced gut microbiota fluctuation. Oral administration of fRG, RG, Rd, or CK also decreased IS-induced AD-like behaviors, blood IL-6 and corticosterone and colonic IL-6 and TNF-levels, and gut dysbiosis, while IS-suppressed hypothalamic dopamine and serotonin levels increased. CONCLUSION: Oral gavage of UCDF caused AD, neuroinflammation, and gastrointestinal inflammation in mice. fRG mitigated AD and colitis in UCDF-exposed mice by the regulation of the microbiota-gut-brain axis and IS-exposed mice by the regulation of the hypothalamic-pituitary-adrenal axis.

PMID:  J Ginseng Res. 2023 Mar ;47(2):193-198. Epub 2022 Dec 5. PMID: 36926605 Abstract Title:  Protective effects of Korean Red Ginseng against toxicity of endocrine-disrupting chemicals. Abstract:  Several chemicals have been developed owing to the progression of industrialization, among which endocrine-disrupting chemicals (EDCs; essential for plastic production) are used as plasticizers and flame retardants. Plastics have become an essential element in modern life because they provide convenience, thus increasing EDCs exposure to humans. EDCs cause adverse effects such as deterioration of reproductive function, cancer, and neurological abnormalities by disrupting the endocrine system and hence are classified as "dangerous substances." Additionally, they are toxic to various organs but continue to be used. Therefore, it is necessary to review the contamination status of EDCs, select potentially hazardous substances for management, and monitor the safety standards. In addition, it is necessary to discover substances that can protect against EDC toxicity and conduct active research on the protective effects of these substances. According to recent research, Korean Red Ginseng (KRG) exhibits protective effects against several toxicities caused by EDCs to humans. In this review, the effects of EDCs on the human body and the role of KRG in protection against EDC toxicity are discussed.

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PMID:  J Ginseng Res. 2023 Mar ;47(2):218-227. Epub 2021 Dec 2. PMID: 36926602 Abstract Title:  Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-B pathway. Abstract:  BACKGROUND: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and Anginduced cardiac fibroblasts (CFs) model.METHODS: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the Ang-induced CFs model.RESULTS: MiR-489 decreased the expression of-SMA, collagen, collagenand myd88, and inhibited the phosphorylation of NF-B p65 in normal CFs and CFs treated with Ang. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-B p65.CONCLUSION: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-B pathway. Ginsenoside Re can ameliorate AMI and Anginduced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-B signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.

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