PMID: 

Med Sci Monit. 2019 Sep 17 ;25:6972-6979. Epub 2019 Sep 17. PMID: 31527568

Abstract Title: 

Ginsenoside Rg3 Reduces Epithelial-Mesenchymal Transition Induced by Transforming Growth Factor-β1 by Inactivation of AKT in HMrSV5 Peritoneal Mesothelial Cells.

Abstract: 

BACKGROUND Ginsenosides, including ginsenoside Rg3, are components of Panax ginseng C.A. Meyer (Araliaceae) used in traditional Chinese medicine. Long-term peritoneal dialysis induces peritoneal fibrosis that impairs ultrafiltration and is associated with epithelial-mesenchymal transition (EMT) of peritoneal cells. This study aimed to investigate the effects of ginsenoside Rg3 on EMT induced by transforming growth factor-ß1 (TGF-ß1) in HMrSV5 human peritoneal mesothelial cells. MATERIAL AND METHODS The cell counting kit-8 (CCK-8) assay measured HMrSV5 cell viability. The expression of EMT markers, E-cadherin, vimentin, and alpha-smooth muscle actin (alpha-SMA) were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The wound-healing assay determined cell migration. The S-phase of the cell cycle was assessed by 5-ethynyl-2'-deoxyuridine (EdU) labeling, and expression of phosphorylated AKT was measured by Western blot. The effect of ginsenoside Rg3 and the AKT activator SC79 onthe TGF-ß1-induced EMT of HMrSV5 cells were evaluated. RESULTS Low concentration of ginsenoside Rg3 did not effect cell viability of HMrSV5 cells. TGF-ß1 treatment decreased the expression of E-cadherin, and increased the expression of vimentin and alpha-SMA and promoted cell migration of HMrSV5cells. However, co-treatment of ginsenoside Rg3 and TGF-ß1 significantly reduced TGF-ß1-induced EMT in HMrSV5 cells. TGF-ß1 increased the phosphorylation of AKT and increased the expression of Smurf2. Ginsenoside Rg3 reduced TGF-ß1-induced activation of AKT and Smurf2. SC79 reversed the effectsof ginsenoside Rg3 on TGF-ß1-induced EMT in HMrSV5 cells. CONCLUSIONS Ginsenoside Rg3 inhibited EMT induced by TGF-ß1 in HMrSV5 human peritoneal mesothelial cells by inhibiting the activation of AKT.

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PMID: 

Oncol Lett. 2019 Oct ;18(4):4160-4166. Epub 2019 Aug 14. PMID: 31579419

Abstract Title: 

Ginsenoside Rh1 inhibits colorectal cancer cell migration and invasionand tumor growth.

Abstract: 

Colorectal cancer (CRC) is the third leading cause of cancer-associated mortality worldwide. Ginsenoside Rh1 (Rh1) is a traditional medicine monomer with antitumor activity; however, the effects of Rh1 in CRC remain to be determined. In the present study, SW620 cells were treated with different concentrations of Rh1. Cell Counting Kit-8, wound healing and Transwell assays were performed to measure cell viability and proliferation, migration and invasion, respectively. Subsequently, the mRNA expression levels of matrix metallopeptidase (MMP)1, MMP3 and tissue inhibitor of metalloproteinases 3 (TIMP3) were detected by reverse transcription-quantitative PCR analysis. In addition, the protein expression levels of MMP1, MMP3, TIMP3, and total or phosphorylated (p-)ERK1/2, P38, JNK were detected by western blotting. Furthermore, tumor growth was examined in a nude mouse xenograft model. The results of the present study indicated that Rh1 was not toxic to CRC cells at various concentrations (0, 50 or 100µM) and treatment durations (24 or 48 h). However, cell proliferation was suppressed by Rh1 in a dose-dependent manner. Rh1 (100 µM) significantly inhibited cell migration and invasion. Additionally, Rh1 suppressed the mRNA and protein expression of MMP1 and MMP3, and promoted TIMP3 expression. Rh1 decreased the ratios of p-P38/P38, p-ERK1/2/ERK1-2 and p-JNK/JNKand, which suggested that Rh1 inactivated the mitogen-activated protein kinase (MAPK) signaling pathway. Notably, Rh1 markedly decreased tumor volume and weight. In conclusion, the present study demonstrated that Rh1 inhibited the proliferation, migration and invasion of CRC cellsand tumor growth. This inhibition was at least partially due to the inhibition of MMP1 and MMP3 expression, the increase in TIMP3 expression level and the MAPK signaling pathway inactivation. Therefore, Rh1 may effectively inhibit the development of CRC as an anticancer drug, and may have a supporting effect during CRC treatment.

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There’s little doubt that CBD has become a way of life—a recent survey found that an estimated 64 million Americans have tried the chemical compound found in the cannabis plant that’s been linked to numerous wellness benefits, from reducing inflammation and sleeplessness to mitigating anxiety and acne. But similar to the supplement industry, CBD is largely unregulated. And with a wave of new cannabis cure-alls hitting the market (vape pens, skin patches, edible confections), uncertainty abounds in the search for a safe, effective product.

That might change: The FDA held its first public hearing on CBD last week, calling on experts to present research and recommendations to help shape potential regulations. Zoe Sigman, the program director for Project CBD, was among those in attendance at Municipal Building 31 in Silver Spring, Maryland, to deliver comments. “It was packed,” she says of the hearing, which lasted for 10 hours and included more than a hundred speakers.

The most compelling takeaway for Sigman? “The contaminants found in CBD products, which don’t contain what they say they contain,” she says, adding that toxicologists found evidence of pesticides, heavy metals, bacteria, and other compounds in widely available products. The problem is rampant: A study from the JAMA Network journal reported that more than two-thirds of CBD products tested by researchers were mislabeled—these items actually had more CBD than listed, or none at all, or other parts from the plant, including tetrahydrocannabinol (known as THC), the main psychoactive derived from cannabis. “There are good people and not-so-good people making CBD products—and no way for consumers to know the difference,” says Sigman.

While the FDA considers how to chart a course forward—Sigman argued for forming a regulatory committee within the FDA that would allow medicinal plant claims based on scientific evidence—consumers will have to advocate for themselves to find quality products. Here, seven points to consider before selecting your next CBD drop, oil, or tincture:

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Credits:
Source: https://www.vogue.com/

News Link: https://www.vogue.com/article/cannabis-cbd-fda-finding-safe-effective-products

The post How Safe Is Your CBD? The FDA Is Asking—And You Should, Too appeared first on AlternativeWellness.

PMID: 

J Gynecol Obstet Hum Reprod. 2019 Sep 26:101642. Epub 2019 Sep 26. PMID: 31563698

Abstract Title: 

Ginsenoside Rg3 attenuates endometriosis by inhibiting the viability of human ectopic endometrial stromal cells through the nuclear factor-kappaB signaling pathway.

Abstract: 

OBJECTIVE: To investigate the effects of ginsenoside Rg3 on human ectopic endometriotic stromal cells in vitro.MATERIALS AND METHODS: Ectopic endometrial tissue specimens were obtained from 6 female patients with ovarian endometriosis who underwent laparoscopic surgical procedures. Endometrial stromal cells derived from isolated ectopic endometriotic lesions were cultured, and the purity and homogeneity of cells were verified by Immunocytochemistry. The effect of Rg3 on cell proliferation was detected by Cell Counting Kit-8 (CCK8). After treatment with Rg3, the protein expression of NF-κB p65 subunit, VEGF, and caspases3 were measured by western blot analysis. Meanwhile, the mRNA expression of NF-κB p65 subunit was determined by Quantitative real-time polymerase chain reaction (RT-PCR).RESULTS: Rg3 inhibited the proliferation of ectopic endometriotic cells in a time- and dose-dependent manner. The treatment with Rg3 significantly diminished the level of NF-κB p65 subunit as well as TNF-α induced nuclear translocation of NF-κB p65 subunit in ectopic endometriotic cells. Moreover, Rg3 upregulated the expression of caspases3 but suppressed the expression of VEGF.CONCLUSION: Our results indicate that Ginsenoside Rg3 suppresses endometriosis by reducing the viability of human ectopic endometrial stromal cells involving the nuclear factor-kappaB signaling pathway in vitro.

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PMID: 

Biomed Pharmacother. 2019 Sep 29 ;120:109487. Epub 2019 Sep 29. PMID: 31577975

Abstract Title: 

Ginsenoside Rb3 regulates energy metabolism and apoptosis in cardiomyocytes via activating PPARα pathway.

Abstract: 

Heart failure (HF) leads to an increase in morbidity and mortality globally. Disorders of energy metabolism and apoptosis of cardiomyocytes are critically involved in the progression of HF. Ginsenoside Rb3 (G-Rb3) is a natural product derived from ginseng that has cardio-protective effect. The pharmacological mechanism of G-Rb3 in the treatment of HF remains to be clarified. In this study, we aimed to explore the regulative effects of G-Rb3 on fatty acids oxidation and apoptosis by in vivo and in vitro studies. Myocardial infarction (MI)-induced HF mice model and a cellular H9C2 injury model was induced by oxygen-glucose deprivation/reperfusion (OGD/R) stimulation. The results showed that G-Rb3 could protect heart functions in MI-induced HF model. G-Rb3 treatment up-regulated expressions of key enzymes involved inβ-oxidation of fatty acids, including carnitine palmitoyltransterase-1α (CPT-1α), acyl-CoA dehydrogenase long chain (ACADL) and the major mitochondrial deacetylase enzyme sirtuin 3 (SIRT3). The upstream transcriptional regulator, peroxisome proliferator-activated receptor α (PPARα), was also up-regulated by G-Rb3 treatment. In vitro study demonstrated that G-Rb3 could protect mitochondrial membrane integrity and exert anti-apoptotic effects, in addition to regulating fatty acids oxidation. Impressively, after cells were co-treated with PPARα inhibitor, the regulative effects of G-Rb3 onenergy metabolism and apoptosis were abrogated. Our study suggests that G-Rb3 is a promising agent and PPARα is potential target in the management of HF.

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PMID: 

Saudi Pharm J. 2019 Jul ;27(5):664-672. Epub 2019 Apr 4. PMID: 31297021

Abstract Title: 

-Sitosterol derived compound from onion husks non-polar fraction reduces quorum sensing controlled virulence and biofilm production.

Abstract: 

Quorum sensing is an important regulatory factor ofvirulence induction such as BF, motility, formations of proteases, pyocyanin, and some toxins. The aim of the current study is to detect the effect of the pet.ether extract from onion husk and compound drive from it on quorum sensing and virulence formations of. Quorum sensing inhibiting effect of the pet.ether extract of onion husk and a compound drive from it, was evaluated byreporter using dilution method as well as an antioxidant by using DPPH. The efficacious of: Quorum sensing inhibiting on pet.ether fraction and compound derived from it, were investigated for their activities toward biofilm and pyocyanin synthesis as well as motility from. The pet.ether fraction and compound derived from it of onion husk exhibited potent antimicrobial, antioxidant and Quorum sensing inhibiting effects. The pet.ether fraction and compound derived from it possesses significant reduction on pyocyanin and biofilm induction of. Moreover, they significantly inhibited swimming motilities of. For the first time, our study showed the medical importance ofL. as antimicrobial, antioxidant as well as Quorum sensing inhibiting and virulence suppressors of. Thus, these might emphasized onL as a natural source for attenuating toxins of the.

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PMID: 

Mol Cell Biochem. 2019 Sep 6. Epub 2019 Sep 6. PMID: 31493190

Abstract Title: 

Cytotoxic and antiproliferative effects of thymoquinone on rat C6 glioma cells depend on oxidative stress.

Abstract: 

Thymoquinone (TQ) is a highly perspective chemotherapeutic agent against gliomas and glioblastomas because of its ability to cross the blood-brain barrier and its selective cytotoxicity for glioblastoma cells compared to primary astrocytes. Here, we tested the hypothesis that TQ-induced mild oxidative stress provokes C6 glioma cell apoptosis through redox-dependent alteration of MAPK proteins. We showed that low concentrations of TQ (20-50 μM) promoted cell-cycle arrest and induced hydrogen peroxide generation as a result of NADH-quinone oxidoreductase 1-catalyzed two-electron reduction of this quinone. Similarly, low concentrations of TQ efficiently conjugated intracellular GSH disturbing redox state of glioma cells and provokingmitochondrial dysfunction. We demonstrated that high concentrations of TQ (70-100 μM) induced reactive oxygen species generation due to its one-electron reduction. TQ provoked apoptosis in C6 glioma cells through mitochondrial potential dissipation and permeability transition pore opening. The identified TQ modes of action on C6 glioma cells open up the possibility of considering it as a promising agent to enhance the sensitivity of cancer cells to standard chemotherapeutic drugs.

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PMID: 

J Histotechnol. 2019 Sep ;42(3):116-127. Epub 2019 Jul 24. PMID: 31492091

Abstract Title: 

Thymoquinone ameliorates oxidative damage and histopathological changes of developing brain neurotoxicity.

Abstract: 

Lead (Pb) toxicity is known to be a chief environmental health issue, especially for pregnant women and young children. Today, the use of medicinal herbs in the treatment of many diseases and different toxic agents has become highly accepted due to their effectiveness and lower costs. Thymoquinone (TQ), which is extracted fromseeds, is a potent antioxidant and anti-inflammatory agent. This study was designed to explore the optional protectivity of TQ against maternal and fetal oxidative stress and brain damage induced by Pb administration. Pregnant rats were distributed into seven groups: control group, TQ group, DMSO group, two groups Pb-treated (160 and 320 ppm), and two groups Pb-treated (160 and 320 ppm) co-treated with TQ. Administration started from gestation day 1 (GD1) to day 20 (GD20) through oral gavage once daily. Lead administration caused a dose-dependent toxicity for both mothers and fetuses. Also, the histopathological assessment of the brains from Pb-treated groups showed marked alterations. Co-treatment of with TQ and Pb caused a significant decrease in Pb levels as compared with those treated with Pb alone and amelioration of histopathological changes in the brains. It was concluded that co-treatment of TQ along with gestational Pb exposure could mitigate the effects against Pb-induced maternal and fetal neurotoxicity.

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PMID: 

Mater Sci Eng C Mater Biol Appl. 2019 Nov ;104:109881. Epub 2019 Jun 11. PMID: 31499940

Abstract Title: 

Thymoquinone loaded mesoporous silica nanoparticles retard cell invasion and enhance in vitro cytotoxicity due to ROS mediated apoptosis in HeLa and MCF-7 cell lines.

Abstract: 

Thymoquinone (TQ) loaded monodispersed mesoporous silica nanoparticles (TQ-MSNPs) with size of 188 ± 3 nm were prepared and characterized using DLS, TEM and FTIR. These TQ-MSNPs overcome the limitations of free TQ like hydrophobicity, low aqueous and photo stability and thus enhance its anticancer activity. In vitro release kinetics showed biphasic drug release where up to 50% was released in first 8 h and subsequently 98% released after 48 h. Enhanced cytotoxicity of TQ-MSNPs was observed against MCF-7 and HeLa cell lines as compared to free TQ. DAPI and Annexin V-FITC/PI staining confirmed the induction of apoptosis in cancer cells following treatment with TQ-MSNPs. Also, TQ-MSNPs exhibited enhanced anti-invasion properties against both cell lines as very low concentration of loaded TQ imparts similar benefits as free TQ. Both TQ and TQ-MSNPs exerted their cytotoxicity via reactive oxygen species (ROS) generation, as addition of an antioxidant NAC attenuated their killing activity.

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PMID: 

Front Cell Infect Microbiol. 2019 ;9:304. Epub 2019 Aug 27. PMID: 31508379

Abstract Title: 

Inhibitory Effect of Thymoquinone onATCC 19115 Biofilm Formation and Virulence Attributes Critical for Human Infection.

Abstract: 

This study aimed to determine the antimicrobial activity of thymoquinone (TQ) against, and to examine its inhibitory effects on biofilm formation, motility, hemolysin production, and attachment-invasion of host cells. The minimum inhibitory concentrations (MICs) of TQ against eight differentstrains ranged from 6.25-12.50μg/mL. Crystal violet staining showed that TQ clearly reduced biofilm biomass at sub-MICs in a dose-dependent manner. Scanning electron microscopy suggested that TQ inhibited biofilm formation on glass slides and induced an apparent collapse of biofilm architecture. At sub-MICs, TQ effectively inhibited the motility ofATCC 19115, and significantly impacted adhesion to and invasion of human colon adenocarcinoma cells as well as the secretion of listeriolysin O. Supporting these findings, real-time quantitative polymerase chain reaction analysis revealed that TQ down-regulated the transcription of genes associated with motility, biofilm formation, hemolysin secretion, and attachment-invasion in host cells. Overall, these findings confirm that TQ has the potential to be used to combatinfection.

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