CAJ | 학술논문

目的：探讨丁酸钠预处理对大鼠缺血/再灌注（I/ R）损伤的影响。方法：大鼠缺血前30 min用丁酸钠（100或300 mg/kg，腹腔注射）处理，结扎冠脉前降支缺血30 min 再灌注4 h；检测乳酸脱氢酶（LDH）、肌酸激酶（CK）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）、丙二醛（MDA）和超氧化物歧化酶（SOD）；应用2，3，5-氯化三苯基四氮（TTC）法检测心梗面积；蛋白免疫印迹法检测高迁移率族蛋白1（HMGB1）表达。结果：再灌注4 h后，相对于对照组，丁酸钠（300 mg/kg）预处理显著减少心梗面积；降低LDH 和CK 的表达水平（P ＜0．05）；抑制 MDA 含量增加，抑制 SOD 含量的减少（P ＜0．05）；也明显抑制 I/R 所诱导的TNF-α、IL-6和HMGB1的表达（均P ＜0．05）。结论：丁酸钠预处理可通过减轻炎症反应进而减轻心肌 I/R损伤。
목적：탐토정산납예처리대대서결혈/재관주（I/ R）손상적영향。방법：대서결혈전30 min용정산납（100혹300 mg/kg，복강주사）처리，결찰관맥전강지결혈30 min 재관주4 h；검측유산탈경매（LDH）、기산격매（CK）、종류배사인자-α（TNF-α）화백세포개소-6（IL-6）、병이철（MDA）화초양화물기화매（SOD）；응용2，3，5-록화삼분기사담（TTC）법검측심경면적；단백면역인적법검측고천이솔족단백1（HMGB1）표체。결과：재관주4 h후，상대우대조조，정산납（300 mg/kg）예처리현저감소심경면적；강저LDH 화CK 적표체수평（P ＜0．05）；억제 MDA 함량증가，억제 SOD 함량적감소（P ＜0．05）；야명현억제 I/R 소유도적TNF-α、IL-6화HMGB1적표체（균P ＜0．05）。결론：정산납예처리가통과감경염증반응진이감경심기 I/R손상。
Objective To investigate the effect of preconditioning with sodium butyrate on myocardial I/R injury. Methods Anesthetized rats were treated with sodium butyrate (100 or 300 mg/kg, i.p.) 30 mins before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. LDH, CK, TNF-α, IL-6, HMGB1, infarct size, MDA and SOD activity were measured. The infracted size was tested by TTC assay; The expression of HMGB1 was observed by western blot. Results After 4 h reperfusion, pretreatment of sodium butyrate (300 mg/kg) could significantly reduce the infarct size and the levels of LDH and CK (P<0.05)comparing to the control group; inhibit the increase of the MDA level and the decrease of the SOD level(P<0.05), also inhibit the expression of TNF-α, IL-6 and HMGB1 (all P < 0.05) induced by I/R. Conclusion Preconditioning of sodium butyrate can attenuate myocardial I/R injury by inhibiting inflammation response.