Objective:Based on the glucose-regulatory protein 78(GRP78)/NOD-like receptor protein 3(NLRP3)signaling pathway to explore the anti-atherosclerosis mechanism of Tianxiangdan through regulation of endoplasmic reticulum stress.Methods:A total of 35 male apolipoprotein E gene knockout(ApoE-/-)mice were randomly divided into model group,atorvastatin group and Tianxiangdan group,with 6 mice in each group.Atherosclerosis model was induced by high fat diet.Another 10 male C57BL/6J mice were selected as the normal group.After 10 weeks of modeling,the corresponding drug treatment was given.The intervention lasted for 12 weeks.Hematoxylin-eosin(HE)staining was used to observe the pathological features of thoracic aorta.Serum interleukin-1 β(IL-1β),interleukin-18(IL18)and reactive oxygen species(ROS)were detected by enzyme-linked immunosorbent assay(ELISA).The positive expression levels of GRP78 and NLRP3 proteins in thoracic aorta were detected by immunohistochemistry(IHC-P).Results:Compared with model group,the expression levels of IL-1β,IL-18 and ROS in atorvastatin group and Tianxiangdan group decreased(P＜0.05 or P＜0.01),the positive expressions of GRP78 and NLRP3 decreased(P＜0.05 or P＜0.01).Conclusion:Tiangdan can effectively improve the inflammatory response of mice with atherosclerotic cardiovascular disease,and its mechanism may be related to the regulation of endoplasmic reticulum stress GRP78/NLRP3 signaling pathway to inhibit the activation of inflammasome and reduce the inflammatory damage of arteriosclerotic disease.
关键词
动脉粥样硬化/天香丹/内质网应激/葡萄糖调节蛋白78/NOD样受体蛋白3/实验研究
Key words
arteriosclerotic cardiovascular disease/Tianxiangdan/endoplasmic reticulum stress/glucose-regulatory protein 78/NOD-like receptor protein 3/experimental study
维普
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