Antifatigue Effect of Panax Notoginseng Leaves Fermented With Microorganisms: In-vitro and In-vivo Evaluation.

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.

Astragalin Inhibits the Proliferation and Migration of Human Colon Cancer HCT116 Cells by Regulating the NF-κB Signaling Pathway.

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.