Moringa oleifera is a commonly used plant with high nutritional and medicinal values. M. oleifera leaves are considered a new food resource in China. However, the biological activities of M. oleifera polysaccharides (MOP) in regulating gut microbiota and alleviating obesity remain obscure. In the present study, we prepared the MOP and evaluated its effects on obesity and gut microbiota in high-fat diet (HFD)-induced C57BL/6J mice. The experimental mice were supplemented with a normal chow diet (NCD group), a high-fat diet (HFD group), and HFD along with MOP at a different dose of 100, 200, and 400 mg/kg/d, respectively. Physiological, histological, biochemical parameters, genes related to lipid metabolism, and gut microbiota composition were compared among five experimental groups. The results showed that MOP supplementation effectively prevented weight gain and lipid accumulation induced by HFD, ameliorated blood lipid levels and insulin resistance, alleviated the secretion of pro-inflammatory cytokines, and regulated the expression of genes related to lipid metabolism and bile acid metabolism. In addition, MOP positively reshaped the gut microbiota composition, significantly increasing the abundance of Bacteroides, norank_f_Ruminococcaceae, and Oscillibacter, while decreasing the relative abundance of Blautia, Alistipes, and Tyzzerella, which are closely associated with obesity. These results demonstrated that MOP supplementation has a protective effect against HFD-induced obesity in mice, which was associated with reshaping the gut microbiota. To the best of our knowledge, this is the first report on the potential of MOP to prevent obesity and modulating gut microbiota, which suggests that MOP can be used as a potential prebiotic.

Astragalin is a flavonoid found in a variety of natural plants. It has anti-inflammatory, anti-oxidant effects and has inhibited effects against several malignant tumor cell types. However, its effects on colon cancer and the molecular mechanisms have remained to be elucidated. In this study, we evaluated the inhibitory effect of astragalin on proliferation and migration of human colon cancer HCT116 cells in vitro and in vivo. Furthermore, we elucidated the mechanism of these effects. The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis (by modulation of Bax, Bcl-2, P53, caspase-3, caspase 6, caspase 7, caspase 8, caspase 9 protein express) and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express). Moreover, astragalin suppressed HCT116 cell migration by inhibiting the expression of matrix metalloproteinases (MMP-2, MMP-9). In addition, astragalin significantly downregulated the expression of key proteins in the NF-κB signaling pathway and inhibited the transcriptional activity of NF-κB P65 stimulated with inflammatory cytokines TNF-α, thereby inhibiting the growth of colon cancer cells in vitro. Our further investigations unveiled astragalin gavage significantly reduced the proliferation of colon cancer xenograft in nude mice, in vivo experiments showed that tumor growth was related to decreased expression of apoptotic proteins in tumor tissues and decreased activity of the NF-κB signaling pathway. In summary, our results indicated that astragalin inhibits the proliferation and growth of colon cancer cells in vivo and in vitro via the NF-κB pathway. Therefore, astragalin maybe become a potential plant-derived antitumor drug for colon cancer.

Moringin [4-(α-L-rhamnosyloxy) benzyl isothiocyanate] is an isothiocyanate from Moringa oleifera seeds. It is the bioactivated form of the glucosinolate precursor glucomoringin with various health benefits. However, few studies have examined the antibacterial activity of moringin. This study aimed to investigate the antimicrobial activity and mechanism of moringin against Listeria monocytogenes. The minimum inhibitory concentration (MIC), and growth curves were used to evaluate the bacteriostatic effect of moringin against L. monocytogenes. Transcriptome analysis by RNA sequencing was performed to elucidate the underlying mechanism of moringin against L. monocytogenes. The transcriptome results were validated. The results showed that moringin inhibited the growth of L. monocytogenes with a MIC of 400 μM. RNA sequencing results showed that the differences in the expression of genes related to the cell wall and membrane biosynthesis, phosphotransferase system (PTS), oxidative stress, energy metabolism, and DNA binding were significantly affected. As with the transcriptome results, the results of the mechanism verification found that moringin damaged the integrity of the cell wall and cell membrane, stimulated oxidative stress, interfered with energy metabolism and DNA replication, and finally led to the death of L. monocytogenes. The present study provides evidence that moringin exhibits strong antimicrobial activity against L. monocytogenes and insight into its potential mechanism.

Fatigue is a common physiological phenomenon caused by many complicated factors. Excessive fatigue will lead to a series of uncomfortable reactions and damage body health. Panax notoginseng leaves (PNL) is a new resource food that good for soothing nerves, nourishing the heart, and strengthening the spleen. Microbial fermentation could increase the content of bio-ingredients and produce new active ingredients. However, the effect of fermented P. notoginseng leaves (FPNL) on antifatigue and the molecular mechanisms remain to be elucidated. Thus, in this study, we evaluated the antifatigue effect of co-fermented P. notoginseng leaves by Saccharomyces cerevisiae and Bacillus subtilis in-vitro and in-vivo, and its mechanism was further elucidated. The results showed that FPNL exhibited higher saponins, organic phenolic acids content, and antioxidant activity than PNL. FPNL improved ISO-induced H9c2 myocardial cell damage by alleviating apoptosis (modulating Bax and Bcl-2 protein expression) and reducing antioxidant activity in-vitro. Moreover, in-vivo experiment showed that FPNL significantly prolonged the weight-loading swimming time of mice. After gavaged FPNL, the levels of liver glycogen (LG) and serum lactate dehydrogenase (LDH) activity were increased in mice. In contrast, the levels of blood urea nitrogen (BUN), lactate acid, and malondialdehyde (MDA) were decreased. In summary, our results indicated that FPNL showed a good antifatigue effect in-vivo and in-vitro.

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