Department of Gastroenterology, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314001, Zhejiang Province, China.
Department of Pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314001, Zhejiang Province, China.
Aging (Albany NY). 2022 Oct 10;14(22):8970-8981. doi: 10.18632/aging.204330.
This study illustrated the liver protection mechanism of ACP from the perspective of autophagy activation. ACP suppressed the inflammatory injury of KCs, and decreased the cell apoptosis rate. After LTG and LC3 staining, ACP promoted lysosomal production, increased LC3 expression, activated autophagy, and suppressed the expression of NLRP3 and inflammatory factors. Under the electron microscope, ACP accelerated the production of autophagosomes. After simultaneous treatment with 3-MA and ACP, the effect of ACP on resisting KC injury decreased, the expression of NLRP3 was up-regulated, and autophagy was suppressed. As discovered in the mouse model of liver injury, ACP inhibited the ALT and AST levels, promoted the occurrence of autophagy, reduced NLRP3 expression and alleviated liver injury. ACP activates autophagy to induce NLRP3 degradation, thus suppressing inflammatory response in liver injury and exerting the liver protection effect, which is one of the mechanisms of action of ACP.
本研究从自噬激活的角度阐述了 ACP 的肝脏保护机制。ACP 抑制了 KCs 的炎症损伤，降低了细胞凋亡率。经 LTG 和 LC3 染色后，ACP 促进溶酶体生成，增加 LC3 表达，激活自噬，抑制 NLRP3 和炎症因子的表达。在电子显微镜下，ACP 加速了自噬体的产生。在用 3-MA 与 ACP 同时处理后，ACP 抵抗 KC 损伤的效果降低，NLRP3 表达上调，自噬受到抑制。在肝损伤的小鼠模型中发现，ACP 抑制 ALT 和 AST 水平，促进自噬发生，降低 NLRP3 表达，减轻肝损伤。ACP 通过激活自噬诱导 NLRP3 降解，从而抑制肝损伤中的炎症反应，发挥肝脏保护作用，这是 ACP 的作用机制之一。
