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目的:探讨玉郎伞查尔酮(YLSC)后处理对大鼠离体心脏缺血/再灌注损伤(I/R)的保护作用及相关信号传导通路机制。方法:将60只雄性SD大鼠随机分为正常组,模型组,YLSC组(5μmol·L~(-1)),AG490组(2μmol·L~(-1)),YLSC+AG490组(YLSC 5μmol·L~(-1)+AG490 2μmol·L~(-1)),每组12只。采用停灌30 min,再灌注120 min的方法制备大鼠离体心脏缺血/再灌注模型。再灌注前10 min给予AG490或YLSC。记录心率(HR),左心室舒张末压(LVEDP)和左室内压最大变化速率(±dp/dtmax)。收集冠脉流出液,测定冠脉流出液中乳酸脱氢酶(LDH)含量。再灌结束后处死大鼠,2,3,5-氯化三苯基四氮唑(TTC)法测定心肌梗死面积,蛋白免疫印迹法(Western blot)检测心肌组织磷酸化Janus激酶2(phosphorylated janus kinase 2,p-JAK2),磷酸化信号转导和转录激活子3(phosphorylated signal transducer and activator of transcription 3,p-STAT3),B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2),Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)蛋白表达量。结果:与模型组比较,YLSC后处理可明显改善心功能,缩小心肌梗死面积,减少LDH含量,减少凋亡及Bax表达水平,上升p-JAK2,p-STAT3及Bcl-2表达水平(P<0.05,P<0.01)。而同时给予YLSC和AG490处理后,血流动力学改善作用减弱,心肌梗死面积,LDH及Bax表达较YLSC组回升,p-JAK2,p-STAT3,Bcl-2的表达较YLSC组降低(P<0.05,P<0.01)。结论:YLSC后处理能减轻大鼠离体心脏缺血/再灌注损伤,其机制可能与激活JAK2/STAT3通路有关。
Objective: To investigate the protective effect of Yulang parachalcone (YLSC) postconditioning on isolated rat heart ischemia/reperfusion injury (I/R) and related signaling pathways. Methods: Sixty male SD rats were randomly divided into normal group, model group, YLSC group (5μmol·L -1), AG490 group (2μmol·L -1), YLSC+AG490 group (YLSC 5μmol·L -1 +AG490 2μmol·L -1), 12 in each group. Rat isolated heart ischemia/reperfusion model was established by stopping the irrigation for 30 min and reperfusion for 120 min. Give AG490 or YLSC 10 min before reperfusion. Heart rate (HR), left ventricular end-diastolic pressure (LVEDP) and maximum rate of left ventricular compression (±dp/dtmax) were recorded. The coronary effluent was collected and the lactate dehydrogenase (LDH) content in the coronary effluent was measured. At the end of reperfusion, the rats were sacrificed. Myocardial infarct size was measured by 2, 3, 5-triphenyltetrazolium chloride (TTC) method. Myocardial tissue phosphorylation of Janus kinase 2 (phosphorylated janus) was detected by Western blot. Kinase 2, p-JAK2), phosphorylated signal transducer and activator of transcription 3 (p-STAT3), B-cell lymphoma-2, Bcl-2 ), Bcl-2 associated X protein (Bax) protein expression. RESULTS: Compared with the model group, YLSC postconditioning significantly improved cardiac function, reduced myocardial infarct size, decreased LDH content, decreased apoptosis and Bax expression levels, and increased p-JAK2, p-STAT3, and Bcl-2 expression levels (P< 0.05, P<0.01). After treatment with YLSC and AG490, the improvement of hemodynamics was weakened, myocardial infarct size, LDH and Bax expression were increased compared with YLSC group, and p-JAK2, p-STAT3, Bcl-2 expression was lower than YLSC group (P< 0.05, P<0.01). CONCLUSION: YLSC postconditioning can reduce isolated rat heart ischemia/reperfusion injury. The mechanism may be related to activation of JAK2/STAT3 pathway.