Ganoderma lucidum polysaccharide can improve the intestinal injury caused by chemotherapy drugs

- Jun 12, 2017 -

[Editor: Jacky] reporter from the recently held by the China Association for Science and Technology journalists and news media meeting was informed that the Department of Medicine, Peking University Department of Pharmacology, Department of Immunology Pharmacology, a research results show that Ganoderma lucidum polysaccharide can significantly improve the chemotherapy drugs methotrexate (MTX) caused by intestinal injury, inhibition of methotrexate caused by intestinal oxidative stress injury, induced intestinal epithelial cell proliferation and migration, and promote the recovery of immune barrier for the clinical treatment of chemotherapy caused by intestinal mucosal injury Provides a new way of thinking. Research results published in the recently published "Chinese Journal of Pharmacology" on. The following are the same as the "

As the most commonly used treatment of malignant tumors, chemotherapy drugs in the killing of tumor cells at the same time, the normal tissue cells, especially cell renewal faster tissue, such as the digestive tract mucosa and bone marrow cells also have significant killing effect, and thus many chemotherapy Drugs easily cause vomiting, constipation, diarrhea and oral ulcers and other gastrointestinal reactions. Among them, the intestinal mucosal barrier injury that intestinal mucositis is a certain dose of anti-cancer drug toxicity, about 40% to 100% of cancer patients will experience chemotherapy-induced intestinal mucositis interference, but still no effective treatment method.

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Ganoderma lucidum in China has more than two thousand years of medicinal history, Ganoderma lucidum polysaccharide (Gl-PS) is the main biological activity of Ganoderma supplier. The pharmacological effects of Ganoderma lucidum polysaccharides have been widely reported, such as inhibition of tumor growth, anti-oxidative damage, liver and hypoglycemic, regulating biological activity and enhance immune response and so on. However, the role of Ganoderma lucidum polysaccharides on gastrointestinal mucosal function is relatively small. The following are the same as the "

Peking University Department of Medicine Department of Pharmacology, Department of Pharmacology, Department of Pharmacology, Professor Lin Zhibin, Associate Professor Li Weidong under the leadership of Ganoderma lucidum polysaccharide in chemotherapy-induced intestinal mucositis in a comprehensive study. They used to give mice for two consecutive days, once a day intraperitoneal injection of methotrexate to simulate the clinical drug damage to the intestinal mucosal barrier model, based on the study of Gl-PS methotrexate caused by intestinal mucosal injury protection effect. The study found that Gl-PS can significantly improve the chemotherapy of methotrexate-induced intestinal morphological damage. Compared with the untreated group, the mice were treated with Gl-PS, the intestinal villi became longer, arranged neatly, the infiltration of inflammation was reduced, and the ultrastructural changes of the intestinal tract were better than those without the Gl-PS group. Gl-PS also inhibited the oxidative stress injury induced by methotrexate, and decreased the content of malondialdehyde (MDA) and the activity of total superoxide dismutase (T-SOD). At the same time, Gl-PS has to promote the recovery of immune barrier, improve plasma levels of secreted IgA and so on. Suggesting that Ganoderma lucidum polysaccharide administration group can improve MTX-induced intestinal mucosal injury in mice. The following are the same as the "

The laboratory further conducted an in vitro experiment and found that Gl-PS can promote the proliferation and migration of intestinal epithelial cells, thereby promoting the recovery of damaged intestinal mucosal barrier. The pro-proliferative effect is related to the activation of c-Myc and ornithine decarboxylase (ODC) mRNA expression, and its promoting migration is independent of transforming growth factor-beta (TGFβ) pathway.