Ya Chen,Yuan Jiang,Xinyu Huang,Lin Chen,Hao Yang,Jian Zhao,Beibei Liang
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China, with a high incidence and mortality rate. Glucose metabolism reprogramming is a major characteristic of tumor cells. Increasing evidence indicates that aerobic glycolysis is associated with tumor growth and insensitivity to chemotherapy. Cordycepin inhibits the growth of HCC cells, but the mechanism is yet to be elucidated. Herein, in vitro and in vivo methods were utilized to investigate the cordycepin-inhibited growth of HCC by regulating the metabolic pathway of aerobic glycolysis. In vitro analyses using colony formation and flow cytometry revealed that cordycepin inhibits HCC cells’ proliferation and promotes apoptosis. In addition, cordycepin reduced the production of lactic acid and pyruvate, reduced the uptake of glucose, and decreased the extracellular acidification in HCC cells. Specifically, cordycepin inhibited the expression of HK2, LDHA, and PKM2 in aerobic glycolysis via the AMPK-Akt pathway. Taken together, these findings revealed that cordycepin reduces the tumor energy supply and decreases lactic acid production, thereby inhibiting the growth of HCC cells by regulating the metabolic pathway of aerobic glycolysis. These findings might provide novel insights into the mechanisms underlying cordycepin-mediated inhibition of tumor growth as well as a new treatment for HCC.
Bound polyphenols (BPs) are critical to the anti-obesity effects of dietary fiber. However, their role in dietary-fiber-mediated intestinal barrier protection remains unclear. In this study, we demonstrated that rice bran insoluble dietary fiber (RIDF) alleviated intestinal barrier damage in high-fat-diet (high-fat diet)-fed mice, and this beneficial effect was dependent on BPs, as it was attenuated in mice treated with polyphenol-removed dietary fiber (RIDF_DF). Furthermore, fecal supernatant transplantation from RIDF-treated (not RIDF_DF-treated) mice alleviated obesity and reshaped the gut microbiota in recipient mice. Additionally, the fecal supernatant enhanced the intestinal barrier function and augmented the synthesis of short-chain fatty acids. Notably, butyrate administration upregulated intestinal tight junction proteins in Caco-2 cells and HFD-fed mice and increased Oscillospira abundance. Mechanistically, butyrate inhibited apoptosis and promoted autophagy, accompanied by alterations in the AMPK-Akt signaling pathway. These results indicate that BPs contribute to the ameliorative effect of RIDF on intestinal damage.
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