p38丝裂原活化蛋白激酶
MAPK/ERK通路
化学
药理学
细胞凋亡
炎症
再灌注损伤
磷酸化
缺血
医学
内科学
生物化学
作者
Xuehui Zhang,Yuhui Wang,Wanli Shen,Shangzhi Ma,Wen Chen,Rong Qi
摘要
Abstract Objective Although Rosa rugosa has been applied for preventing coronary artery disease, the pharmacological mechanism is little explored. In this study, the effects and mechanisms of Rosa rugosa flavonoids ( RRF ) on myocardial ischemia reperfusion injury ( MIRI ) were investigated. Methods Mice were pretreated by intragastric administration of 600 mg/kg RRF for 7 days. Then MIRI was induced by 45 minutes coronary artery ligation and 3 hours reperfusion. Myocardial infarct size ( MIS ) and histopathology, activities of myocardial enzymes, and effects of RRF on inflammation and apoptosis were evaluated. Results Pretreating the mice with RRF significantly reduced MIS and inhibited activity of plasma myocardial enzymes. Activity of the enzymes associated with anti‐oxidation, SOD , and TEAC , and mRNA expression of NOX 2 were significantly elevated. RRF pretreatment significantly decreased the translocation of p65 from the cytoplasm into the nucleus and reduced the expression of the pro‐inflammatory cytokines, IL ‐6 and IL ‐1β. RRF pretreatment also significantly prevented the expression of caspase‐3 and Bax, and increased the expression of Bcl‐2. And RRF inhibited the phosphorylation of JNK and p38 MAPK . Conclusions RRF significantly inhibited MIRI through anti‐oxidative, anti‐inflammatory, and anti‐apoptosis effects, and mechanisms were associated with its inhibition on phosphorylation of JNK and p38 MAPK .
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