Liu Qian, Li Yuanyuan, Li Junqing, Zhou Junying
Altern Ther Health Med. 2024 Dec;30(12):230-235.
To investigate glycyrrhizin's effects and molecular mechanisms on the progression of alcoholic fatty liver.
An alcoholic fatty liver model was established, followed by the administration of glycyrrhizin ammonium (20 mg/kg). Liver tissue pathological changes were observed using oil red O staining, and pyroptotic bodies were observed using transmission electron microscopy. Western blot was used to detect the expression of related proteins. To establish a model of alcoholic fatty liver cells to explore the molecular mechanism of glycolic acid in this disease.
Glycyrrhizin ammonium reduced the area of oil red staining in liver tissue and the number of pyroptotic bodies decreased the relative protein expression of NOX2, NOX3, p-SYK, STING, p-PDE4B, NLRP3, IL-1β, GSDMD, Caspase-1, and Caspase-4, and increased the relative protein expression of p-SHP1 and Nrf2.
Glycyrrhizin ameliorates the progression of alcoholic fatty liver by modulating the SHP1/SYK signaling pathway in macrophages, thereby inhibiting hepatic lipid peroxidation and pyroptosis.
探讨甘草酸对酒精性脂肪肝进展的影响及其分子机制。
建立酒精性脂肪肝模型，随后给予甘草酸铵（20mg/kg）。采用油红O染色观察肝组织病理变化，用透射电子显微镜观察焦亡小体。采用蛋白质印迹法检测相关蛋白的表达。建立酒精性脂肪肝细胞模型以探究甘草酸在该疾病中的分子机制。
甘草酸铵减少了肝组织油红染色面积，焦亡小体数量减少，NOX2、NOX3、p-SYK、STING、p-PDE4B、NLRP3、IL-1β、GSDMD、Caspase-1和Caspase-4的相对蛋白表达降低，p-SHP1和Nrf2的相对蛋白表达增加。
甘草酸通过调节巨噬细胞中的SHP1/SYK信号通路改善酒精性脂肪肝的进展，从而抑制肝脏脂质过氧化和焦亡。
