Hu Xiaorong, Zhang Kai, Xu Changwu, Chen Zhiqaing, Jiang Hong
Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Department of Cardiology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei 435000, P.R. China.
Exp Ther Med. 2014 Jul;8(1):229-232. doi: 10.3892/etm.2014.1726. Epub 2014 May 20.
High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R.
高迁移率族蛋白B1（HMGB1）在心肌缺血/再灌注（I/R）损伤中起重要作用。丁酸钠作为组蛋白脱乙酰酶抑制剂，已被证明可抑制HMGB1表达。在本研究中，探讨了丁酸钠对大鼠心肌I/R损伤的影响。在诱导缺血前30分钟，对麻醉的雄性大鼠腹腔注射丁酸钠（100或300mg/kg）。然后使大鼠缺血30分钟，随后再灌注4小时。接着测量梗死面积、乳酸脱氢酶（LDH）、肌酸激酶（CK）和超氧化物歧化酶（SOD）活性以及丙二醛（MDA）水平。使用蛋白质免疫印迹分析评估HMGB1的表达。结果表明，丁酸钠（300mg/kg）预处理可显著减小梗死面积，以及降低LDH和CK水平（P<0.05）。此外，丁酸钠（300mg/kg）可显著抑制I/R诱导的MDA水平升高和SOD水平降低（P<0.05）。此外，发现丁酸钠（300mg/kg）处理可显著抑制I/R损伤诱导的TNF-α、IL-6和HMGB1表达（P<0.05）。总之，本研究结果表明，丁酸钠预处理可能通过抑制心肌I/R期间炎症介质的表达来减轻心肌I/R损伤。
