目的 探讨丹参酮II_A（TA）对再灌注致心律失常的改善作用及机制。方法 取60只SD大鼠随机分为6组：对照组，模型组，TA低、高剂量（10、20 mg·^kg-1）组，蛋白激酶C （PKC）激活剂PMA （5 mg·^kg-1）组，TA （20 mg·^kg-1）联合PKC抑制剂Rottlerin （5 mg·^kg-1）组，每组10只。构建SD大鼠心肌缺血再灌注（I/R）模型，缺血30 min再灌注30 min；再灌注期间记录各组小鼠Ⅱ导联心电图并对再灌注后心律失常严重性进行评分；再灌注结束后，取颈静脉血采用试剂盒检测心肌损伤指标肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）、天冬氨酸转氨酶（AST）和心肌肌钙蛋白（cTnT）水平；取左心室心脏组织，使用试剂盒检测丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性，实时荧光定量PCR（qRT-PCR）法检测PKC、缝隙连接蛋白43（Cx43）mRNA表达，Western blotting法检测PKC、Cx43蛋白表达水平和磷酸化水平。结果 与模型组比较，TA 2个剂量组和PKC激活剂PMA组CK-MB、LDH、AST、cTnT、MDA水平均显著降低，SOD活性显著升高，室性早搏（PVB）次数、室性心动过速（VT）次数和持续时间以及心室颤动（VF）次数和持续时间显著减少，心律失常评分显著降低，差异均有统计学意义（P＜0.05、0.01、0.001） ；而TA联合PKC抑制剂组显著削弱TA的作用（P＜0.05、0.01、0.001） ；与模型组相比，TA 2个剂量组和PMA组Cx43 mRNA表达和磷酸化水平显著升高（P＜0.01、0.001） ，而PKC抑制剂使TA的作用显著减弱（P＜0.05、0.001）。结论 TA通过激活PKC调控Cx43表达和磷酸化而改善再灌注后心律失常，减轻心肌I/R损伤。

Objective To investigate the effect and mechanism of tanshinone II_A (TA) on reperfusion arrhythmia. Methods Totally 60 SD rats were randomly divided into six groups:control group, model group, TA low and high dose (10 and 20 mg·kg^-1) group, PKC activator group PMA (5 mg·kg^-1) and TA (20 mg·kg^-1) combined with PKC inhibitor Rottlerin (5 mg·kg^-1) group, 10 in each group. The model of myocardial ischemia/reperfusion (I/R) was established in SD rats, which lasted for 30 min and 30 min respectively. Recorded the lead II electrocardiogram of each group of mice during reperfusion and scored the severity of arrhythmia after reperfusion. At the end of reperfusion, the levels of creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and cardiac troponin (cTnT) in the jugular vein blood were measured by Elisa kit. The contents of malondialdehyde (MDA) and the activity of superoxide dismutase superoxide dismutase (SOD) were detected by kit. The mRNA levels of protein kinase C (PKC), and gap junction protein 43 (Cx43) were detected by real time fluorescence quantitative PCR (qRT-PCR). The protein levels of PKC, phosphorylated PKC, Cx43 and phosphorylated Cx43 were detected by Western blotting. Results Compared with the model group, the contents of CK-MB, LDH, AST, cTnT and MDA in TA two dose groups and PKC activator group were significantly decreased, while the activity of SOD was increased, the frequency of premature ventricular beats (PVB), the frequency and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) were significantly reduced, the differences were statistically significant (P＜0.05, 0.01, 0.001). TA combined with PKC inhibitor could weaken the abovementioned effects of TA (P＜0.05, 0.01, 0.001). Compared with the model group, the levels of Cx43 mRNA and phosphorylated Cx43 were increased in the two TA dose groups (P＜0.01, 0.001), but the effect was attenuated by PKC inhibitor (P＜0.05, 0.001). Conclusion TA ameliorates reperfusion arrhythmia and myocardial I/R injury by activating PKC to regulate CX43 expression and phosphorylation.

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江苏省高等学校基础科学（自然科学）面上基金资助项目（21KJB310001）；南京医科大学科技发展基金资助项目（NMUB2020039）；连云港市重点研发计划基金资助项目（SF2249）