Wu Lei, Liu Xiao-hua, Wang Tian-hui, Duan Rui-feng, Zhou Xue-si, Liu Hong-tao, Zhang Zhi-qing
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2015 May;31(3):193-6.
To observe the protective effects of histone deacetylase inhibitor on stress-induced myocardial injury.
Healthy male Wistar rats were randomly divided into 3 groups( n = 6), and the stress-induced myocardial injury model was established with chronic restraint stress method. The protective effects of histone deacetylase inhibitor on stress-induced myocardial injury were observed with Trichostatin A (TSA) intervention. Histone acetylation levels in myocardium of rats were detected by Western blot method, spectrophotometry method was used to dynamically determine the activity of rat serum lactate dehydrogenase (LDH), serum creatine kinase isoenzyme-MB (CK-MB) and Caspase 3, and nagar Olsen staining were used to observe the early myocardial damage.
Restraint stress could significantly reduce the level of histone acetylation of myocardium in rats, and TSA intervention could inhibit the stress-induced reduction of myocardial levels of histone acetylation. Restraint stress could cause the significant increase of serum LDH activity ( P < 0.05), serum CK-MB activity ( P < 0.05), and the Caspase 3 activity of myocardial tissue (P < 0.05), and early myocardial damage also occurred during restraint stress. ISA intervention could significantly reduce the serum LDH activity (P < 0.05), the serum CK-MB activity (P < 0.05), the activity of myocardial tissue caspase 3 induced by restraint stress (P < 0.05), and the stress-induced myocardial injury was also attenuated by TSA intervention.
The histone deacetylase inhibitor TSA can protect stress-induced myocardial injury.
观察组蛋白去乙酰化酶抑制剂对应激性心肌损伤的保护作用。
将健康雄性Wistar大鼠随机分为3组（n = 6），采用慢性束缚应激法建立应激性心肌损伤模型。通过曲古抑菌素A（TSA）干预观察组蛋白去乙酰化酶抑制剂对应激性心肌损伤的保护作用。采用蛋白质免疫印迹法检测大鼠心肌组织中的组蛋白乙酰化水平，用分光光度法动态测定大鼠血清乳酸脱氢酶（LDH）、血清肌酸激酶同工酶-MB（CK-MB）及Caspase 3活性，用苏木精-伊红染色观察早期心肌损伤情况。
束缚应激可显著降低大鼠心肌组织中的组蛋白乙酰化水平，TSA干预可抑制应激所致的心肌组蛋白乙酰化水平降低。束缚应激可导致血清LDH活性显著升高（P < 0.05）、血清CK-MB活性显著升高（P < 0.05）以及心肌组织Caspase 3活性显著升高（P < 0.05），且束缚应激期间还出现了早期心肌损伤。TSA干预可显著降低血清LDH活性（P < 0.05）、血清CK-MB活性（P < 0.05）、束缚应激诱导的心肌组织caspase 3活性（P < 0.05），TSA干预也减轻了应激性心肌损伤。
组蛋白去乙酰化酶抑制剂TSA可保护应激性心肌损伤。
