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Rosa rugosa flavonoids alleviate myocardial ischemia reperfusion injury in mice by suppressing JNK and p38 MAPK

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
出处
期刊:Microcirculation [Wiley]
卷期号:24 (7) 被引量:23
标识
DOI:10.1111/micc.12385
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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