STUDY ON ANTI-CANCER EFFECT AND MECHANISM OF REFINED POLYSACCHARIDE FROM CORDYCEPS SINENSIS MYCELIUM

Abstract

Objective: In this study, the inhibitory effect of refined polysaccharides from Cordyceps sinensis mycelium on human tumor growth in vivo, the attenuation and synergistic effect of chemotherapy drug cyclophosphamide and the mechanism of action in vitro were studied. Methods: The refined polysaccharide was extracted from the mycelium of Cordyceps sinensis, and the human hepatoma HepG2 cells were cultured and transplanted into the left forelimb of nude mice. The tumor volume was observed to increase to 100 mm³ and randomly divided into groups. Different concentrations of Cordyceps sinensis mycelium polysaccharide were administered to tumor-bearing nude mice alone, and different concentrations of polysaccharide combined with cyclophosphamide were administered to tumor-bearing nude mice. When the tumor volume of the model group reached 2000 mm³, the anatomy was taken, the weight of the tumor and the main organs was weighed, and the blood routine and blood biochemistry were measured. Elisa method was used to determine the concentration of cytokines such as TNF-α, IL-6, IL-β and VEGF in serum. HE staining was performed on the main organs such as liver, kidney and spleen. HepG2 cells in logarithmic growth phase were treated with different concentrations of Cordyceps sinensis mycelium polysaccharide solution. CCK8 method was used to detect cell viability. Western blotting was used to detect the expression of PI3K-AKT-mTOR signaling pathway. The expression of PI3K, p-PI3K, AKT, p-AKT, mTOR, p-mTOR, BCL-2 and BAX proteins was determined. Results: The purified polysaccharides of Cordyceps sinensis mycelia significantly inhibited tumor growth, promoted tumor cell apoptosis, enhanced immune regulation, and improved the inflammatory response of major organs in animals. In vitro cell experiments, CCK8 results showed that Cordyceps sinensis mycelia polysaccharides inhibited the growth and proliferation of human hepatocellular carcinoma HepG2 cells, which may play a role by regulating the PI3K-AKT-mTOR signaling pathway