目的 考察靈仙新苷對大鼠心肌缺血再灌注損傷（MIRI）的保護作用，并闡述可能的作用機制。方法 SD大鼠隨機分為6組：假手術組、模型組、丹參酮Ⅱ_A（陽性藥，16 mg/kg）組和靈仙新苷低、中、高（8、16、32 mg/kg）組，連續(xù)ig給藥7 d；采用結扎冠狀動脈左前降支法制備大鼠MIRI模型，缺血40 min再灌120 min；試劑盒法檢測MIRI大鼠血清腫瘤壞死因子-α（TNF-α）、白介素-1β（IL-1β）、白介素-6（IL-6）水平；TTC染色法檢測心肌梗死率，流式細胞術檢測心肌細胞凋亡率；Western blotting法檢測心肌組織中Bcl-2、Bax、TNF-α及Caspase-3的蛋白表達水平。結果 與模型組比較，靈仙新苷（8、16、32 mg/kg）顯著降低MIRI模型大鼠血清中TNF-α、IL-1β、IL-6水平，心肌梗死率和心肌細胞凋亡率；明顯上調Bcl-2蛋白表達水平，下調Bax、TNF-α、Caspase-3蛋白表達水平，且均具有顯著性差異（P<0.05、0.01）。結論 靈仙新苷對MIRI大鼠心肌具有保護作用，其機制可能與抑制TNF-α，調節(jié)Bcl-2/Bax蛋白平衡，減少MIRI誘導的心肌細胞凋亡有關。

Objective To investigate the protective effects of clematichinenoside (AR) on myocardial ischemia-reperfusion injury (MIRI) in rats and elucidate the underlying mechanism. Methods SD rats were randomly divided into six groups:sham, model, Tanshinone ⅡA (positive control, 16 mg/kg), and AR (8, 16, 32 mg/kg) groups. Drug was given for seven consecutive days before the operation by ig method. Animal MIRI model was established by ligation of left anterior descending coronary artery (LAD). Rats were sacrificed after 40 min ischemia and 120 min reperfusion. TNF-α、IL-1β, and IL-6 in serum were measured. Myocardial infarct rate and cardiomyocyte apoptosis rate in MIRI rats were observed by TTC staining and flow cytometry, respectively. Western blotting was used to detect the expression of Bcl-2, Bax, TNF-α, and Caspase-3 in myocardial tissue. Results Compared with model group, AR at 8, 16 and 32 mg/kg reduced the TNF-α, IL-1β, and IL-6 in serum, myocardial infarct rate, and cardiomyocyte apoptosis rate. AR could up-regulate Bcl-2 and down-regulate protein expression levels of Bax, TNF-α and Caspase-3, and the differences were significant (P<0.05, 0.01). Conclusion AR plays an important role in cardioprotection and anti-apoptosis against the ischemia and reperfusion injury in rats. The mechanism could involve in inhibition of TNF-α, regulation of Bcl-2/Bax protein balance and reduction of apoptosis induced by ischemia-reperfusion injury.

新疆維吾爾自治區(qū)自然科學基金資助項目（2015211C001）