التفاصيل البيبلوغرافية
| العنوان: |
Ganoderic acid A alleviates myocardial ischemia-reperfusion injury in rats by regulating JAK2/STAT3/NF-κB pathway. |
| المؤلفون: |
Zhang, Yujian1 (AUTHOR), Shi, Kejian1 (AUTHOR), Lin, Tingting1 (AUTHOR), Xia, Fangfang1 (AUTHOR), Cai, Yaoyao1 (AUTHOR), Ye, Yingchao1 (AUTHOR), Liu, Le1 (AUTHOR) lle2@163.com, Liu, Fuli1 (AUTHOR) liufulimz@163.com |
| المصدر: |
International Immunopharmacology. Jul2020, Vol. 84, pN.PAG-N.PAG. 1p. |
| مصطلحات موضوعية: |
*MYOCARDIAL reperfusion, *CREATINE kinase, *LACTATE dehydrogenase, *MYOCARDIAL infarction, *RATS, *WOUNDS & injuries, *GIBBERELLINS, *STAT proteins |
| مستخلص: |
• The effects of GA on myocardial ischemia-reperfusion injury were investigated. • GA has cardioprotective effects. • The effects may exert through the JAK2/STAT3/NF-κB signaling pathway. This study aimed to investigate the protective effect of Ganoderic acid A (GA) on myocardial ischemia-reperfusion (MIR) injury. The myocardial injury model in rats was established by ligating left anterior descending coronary artery. We measured cardiac hemodynamic, antioxidant enzyme activity, and various biochemical indexes of myocardial tissue, and evaluated myocardial infarction and damage. Further, the expression of JAK2/STAT3/NF-κB signaling pathway-related proteins in myocardial tissue was measured by western blot. The results showed that the myocardial infarction extention was obviously reduced upon GA treatment. Compared with the control group, ischemia-reperfusion rats showed significant increase in lactate dehydrogenase (LDH) and creatine Kinase (CK), which were significantly decreased in GA group. Besides, GA pretreatment effectively decreased the levels of inflammatory cytokines in serum. The phosphorylation of Janus Kinase 2 (JAK2), signal transducer and activator of transcription (STAT3) and Nuclear factor-κB (NF-κB) in reperfusion group were significantly higher than that in control group, which were reversed upon GA treatment. In conclusion, GA may reduce myocardial injury by regulating JAK2/STAT3/NF-κB pathway. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
Academic Search Index |
