目的 探討丹參酮II_A（TA）對再灌注致心律失常的改善作用及機制。方法 取60只SD大鼠隨機分為6組：對照組，模型組，TA低、高劑量（10、20 mg·^kg-1）組，蛋白激酶C （PKC）激活劑PMA （5 mg·^kg-1）組，TA （20 mg·^kg-1）聯(lián)合PKC抑制劑Rottlerin （5 mg·^kg-1）組，每組10只。構(gòu)建SD大鼠心肌缺血再灌注（I/R）模型，缺血30 min再灌注30 min；再灌注期間記錄各組小鼠Ⅱ?qū)?lián)心電圖并對再灌注后心律失常嚴重性進行評分；再灌注結(jié)束后，取頸靜脈血采用試劑盒檢測心肌損傷指標(biāo)肌酸激酶同工酶（CK-MB）、乳酸脫氫酶（LDH）、天冬氨酸轉(zhuǎn)氨酶（AST）和心肌肌鈣蛋白（cTnT）水平；取左心室心臟組織，使用試劑盒檢測丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性，實時熒光定量PCR（qRT-PCR）法檢測PKC、縫隙連接蛋白43（Cx43）mRNA表達，Western blotting法檢測PKC、Cx43蛋白表達水平和磷酸化水平。結(jié)果 與模型組比較，TA 2個劑量組和PKC激活劑PMA組CK-MB、LDH、AST、cTnT、MDA水平均顯著降低，SOD活性顯著升高，室性早搏（PVB）次數(shù)、室性心動過速（VT）次數(shù)和持續(xù)時間以及心室顫動（VF）次數(shù)和持續(xù)時間顯著減少，心律失常評分顯著降低，差異均有統(tǒng)計學(xué)意義（P＜0.05、0.01、0.001） ；而TA聯(lián)合PKC抑制劑組顯著削弱TA的作用（P＜0.05、0.01、0.001） ；與模型組相比，TA 2個劑量組和PMA組Cx43 mRNA表達和磷酸化水平顯著升高（P＜0.01、0.001） ，而PKC抑制劑使TA的作用顯著減弱（P＜0.05、0.001）。結(jié)論 TA通過激活PKC調(diào)控Cx43表達和磷酸化而改善再灌注后心律失常，減輕心肌I/R損傷。

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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江蘇省高等學(xué)?；A(chǔ)科學(xué)（自然科學(xué)）面上基金資助項目（21KJB310001）；南京醫(yī)科大學(xué)科技發(fā)展基金資助項目（NMUB2020039）；連云港市重點研發(fā)計劃基金資助項目（SF2249）