Red cabbage juice-mediated gut microbiota modulation improves intestinal epithelial homeostasis and ameliorates colitis.

Gut microbiota plays a crucial role in inflammatory bowel disease (IBD) and has therapeutic benefits. Thus, targeting the gut microbiota is a promising therapeutic approach for IBD treatment. We recently found that red cabbage juice (RCJ) ameliorates dextran sulfate sodium (DSS)-induced colitis in mice. However, the underlying mechanisms remain unknown. The current study investigated the modulation of gut microbiota in response to treatment with RCJ to ameliorate the DSS colitis. The initial results demonstrated that mice treated with DSS + RCJ showed increased body weight and decreased diarrhea and blood in feces compared to the DSS alone group. RCJ ameliorated colitis by regulating the intestinal barrier function by reducing the number of apoptotic cells, improving colonic protective mucin, and increasing tight junction protein in RCJ + DSS groups compared to the DSS group. Short-gun metagenomic analysis revealed significant enrichment of short-chain fatty acid (SCFAs)-producing bacteria (Butyrivibrio, Ruminococcaceae, Acetatifactor muris, Rosburia Sp. CAG:303 , Dorea Sp. 5-2) increased PPAR-© activation, leading to repression of the nuclear factor κB (NFκB) signaling pathway, thus decreasing the production of crucial inflammatory cytokines and chemokines in the RCJ + DSS groups compared to the DSS group. Pathway abundance analysis showed an increased abundance of the SCFA pathway, reduced histidine degradation ( Bacteroides sartorii, and Bacteroides caecimuris ), and LCFA production in the RCJ+DSS treated group, suggesting the promotion of good colonic health. Furthermore, increased T-reg (FOXP3+) cells in the colon were due to SCFAs produced by the gut microbiota, which was corroborated by an increase in IL-10, a vital anti-inflammatory cytokine. Thus, our study provides the first evidence that RCJ ameliorates colonic inflammation by modulating the gut microbiota.

Gut microbiota: a non-target victim of pesticide-induced toxicity.

The human gut microbiota can be potentially disrupted due to exposure of various environmental contaminants, including pesticides. These contaminants enter into non-target species in multiple ways and cause potential health risks. The gut microbiota-derived metabolites have a significant role in maintaining the host's health by regulating metabolic homeostasis. An imbalance in this homeostasis can result in the development of various diseases and their pathogenesis. Pesticides have hazardous effects on the host's gut microbiota, which is evident in a few recent studies. Therefore, there is an urgent need to explore the effect of pesticide on gut microbiota-mediated metabolic changes in the host, which may provide a better understanding of pesticide-induced toxicity. The present review summarizes the pesticide-induced effects on gut microbiota, which in turn, induces changes in the release of their secondary metabolites that could lead to various host health effects.

Red Cabbage Juice-Mediated Gut Microbiota Modulation Improves Intestinal Epithelial Homeostasis and Ameliorates Colitis.

Gut microbiota plays a crucial role in inflammatory bowel diseases (IBD) and can potentially prevent IBD through microbial-derived metabolites, making it a promising therapeutic avenue. Recent evidence suggests that despite an unclear underlying mechanism, red cabbage juice (RCJ) alleviates Dextran Sodium Sulfate (DSS)-induced colitis in mice. Thus, the study aims to unravel the molecular mechanism by which RCJ modulates the gut microbiota to alleviate DSS-induced colitis in mice. Using C57BL/6J mice, we evaluated RCJ's protective role in DSS-induced colitis through two cycles of 3% DSS. Mice were daily gavaged with PBS or RCJ until the endpoint, and gut microbiota composition was analyzed via shotgun metagenomics. RCJ treatment significantly improved body weight (p ≤ 0.001), survival in mice (p < 0.001) and reduced disease activity index (DAI) scores. Further, RCJ improved colonic barrier integrity by enhancing the expression of protective colonic mucins (p < 0.001) and tight junction proteins (p ≤ 0.01) in RCJ + DSS-treated mice compared to the DSS group. Shotgun metagenomic analysis revealed an enrichment of short-chain fatty acids (SCFAs)-producing bacteria (p < 0.05), leading to increased Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) activation (p ≤ 0.001). This, in turn, resulted in repression of the nuclear factor κB (NFκB) signaling pathway, causing decreased production of inflammatory cytokines and chemokines. Our study demonstrates colitis remission in a DSS-induced mouse model, showcasing RCJ as a potential modulator for gut microbiota and metabolites, with promising implications for IBD prevention and treatment.

Carvacrol Promotes Cell Cycle Arrest and Apoptosis through PI3K/AKT Signaling Pathway in MCF-7 Breast Cancer Cells / 中国结合医学杂志

OBJECTIVE@#To examine the role of carvacrol in modulating PI3K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 cells.@*METHODS@#MTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol (0-250 p mol/L) at different time points (24 and 48 h). The nuclear morphology was assessed in MCF-7 cells with propidium iodide (PI) and acridine orange/ethidium bromide (AO/EB) staining and analyzed by fluorescence microscopy. Events like cell cycle arrest, apoptosis was observed by flow cytometric analysis and expressions of p-Rb, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, Bax, Bcl-2, PI3K/p-AKT was analyzed by immunoblot.@*RESULTS@#Carvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200 µmol/L at 24 and 48 h (P<0.05). importantly, there was a significant increase in the accumulation of the G@*CONCLUSION@#Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.

Apoptotic role of marine sponge symbiont Bacillus subtilis NMK17 through the activation of caspase-3 in human breast cancer cell line.

The aim of the present study was to evaluate the diverse potential biological activity of partially purified crude extract (PPCEBS) of marine Bacillus subtilis NMK17 associated with marine sponge Clathria frondifera. Symbionts were isolated from a marine sponge, only the potential strain which exhibited apoptosis was sequenced using 16S rRNA and extract of the active strain was subjected to purification using HPLC. The potential pro-apoptotic role of PPCEBS was investigated in MCF-7 human breast cancer cell line for cytotoxicity by MTT assay, which showed dose-dependent cytotoxicity on 24 h of exposure. The apoptotic findings demonstrated that PPCEBS significantly induces apoptosis, which was characterised by apoptotic morphological changes. Further, an increased expression of the Caspase 3 and Bax whereas decreased Bcl-2 was confirmed by immunofluorescence and western blotting analysis in MCF-7 cell line, which revealed that PPCEBS has potent apoptosis-inducing property. Added to the desirable apoptotic activity, PPCEBS exhibited excellent antibacterial and antioxidant activities too. The pharmacological effect of the marine sponge-associated bacteria from Gulf of Mannar India needs further attention in discovering new bioactive compounds. Our results suggested that the compounds present in the PPCEBS in marine bacterial B. subtilis NMK17 could be candidates for developing an apoptosis-specific drug with minimal toxicity. This study indicated that marine sponge-associated bacteria could be a good source to find the cytotoxic metabolites which would induce apoptosis and cause cancer cell death. Also, this study explores that marine natural products as a potential source of pharmaceuticals.