结肠炎
p38丝裂原活化蛋白激酶
MAPK/ERK通路
伞菌纲
药理学
炎症性肠病
激酶
医学
磷酸化
蛋白激酶B
传统医学
化学
免疫学
生物
内科学
生物化学
疾病
古生物学
擔子菌門
作者
Yingying Zhao,Liangchen Zhu
标识
DOI:10.1615/intjmedmushrooms.2023049699
摘要
The compound ganoderma lucidum spore powder (GLSP) has emerged as an anti-inflammatory and anti-oxidative regulator. In this study, we explored the roles of GLSP against dextran sulfate sodium (DSS)-induced mouse colitis that can mimic human inflammatory bowel disease (IBD). GLSP was administered by oral gavage at a dosage of 150 mg/kg/day to the acute colitis mice induced by DSS. The DSS-induced mouse weight loss, colonic shortening, diarrhea and bloody stool were observably alleviated after GLSP treatment. The lesion of macroscopic and microscopic signs of the disease was reduced significantly and DSS-induced gut barrier dysfunction was restored via increasing the level of claudin-1, ZO1, Occu, and ZO2 with GLSP. Meanwhile, the levels of IL-6, TNF-α, IL-1β, and IL-18 in the colon were reduced in the GLSP-treated groups. In addition, phosphorylation of the MAPKs ERK1/2, p38, and AKT was suppressed after GLSP treatment. All these results demonstrated that GLSP owned a protective effect on DSS-induced colitis by inhibition of MAPK pathway, which provides a promising therapeutic approach for the treatment of colitis.
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