CAJ | 학술논문

目的观察经过大黄素预处理对大鼠心肌细胞缺血再灌注损伤的保护作用.方法将30只健康SD雄性大鼠随机分为5组,即假手术组(A组,n=6)、心肌缺血再灌注损伤模型组(B组,n=6)、大黄素灌胃预处理组(C组:20 mg/kg;D组:40 mg/kg;E组:60 mg/kg).除A组外均建立在体大鼠心肌缺血再灌注损伤模型.采用苏木素-伊红(HE)染色法观察心肌细胞病理学改变;反转录-聚合酶链反应(RT-PCR)法测定凋亡相关基因B细胞淋巴瘤/白血病-2 (bcl-2)、bcl-2相关X蛋白(bax)、半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3 mRNA表达水平,检测大鼠心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)水平的变化.结果与A组比较,B组和各预处理组均出现明确的心肌缺血和心肌梗死区域;各预处理组心肌细胞中bcl-2 mRNA表达水平以及SOD、MDA活性均较B组[(1.73±0.21)、(33.15 ±3.51) U/(mg·pro)]显著提高(P＜0.01),bax和Caspase-3的mRNA表达水平以及MDA含量较B组[(4.70±0.37)、(4.61±0.52)、(6.87±0.34) nmol/(mg· pro)]明显降低(P＜0.01).结论大黄素能够一定程度抑制缺血再灌注损伤诱导的心肌细胞凋亡作用,减轻再灌注造成的损伤,具有较好的心肌保护作用.
목적 관찰경과대황소예처리대대서심기세포결혈재관주손상적보호작용.방법 장30지건강SD웅성대서수궤분위5조,즉가수술조(A조,n=6)、심기결혈재관주손상모형조(B조,n=6)、대황소관위예처리조(C조:20 mg/kg;D조:40 mg/kg;E조:60 mg/kg).제A조외균건립재체대서심기결혈재관주손상모형.채용소목소-이홍(HE)염색법관찰심기세포병이학개변;반전록-취합매련반응(RT-PCR)법측정조망상관기인B세포림파류/백혈병-2 (bcl-2)、bcl-2상관X단백(bax)、반광안선천동안산특이성단백매(Caspase)-3 mRNA표체수평,검측대서심기조직중초양화물기화매(SOD)、병이철(MDA)수평적변화.결과 여A조비교,B조화각예처리조균출현명학적심기결혈화심기경사구역;각예처리조심기세포중bcl-2 mRNA표체수평이급SOD、MDA활성균교B조[(1.73±0.21)、(33.15 ±3.51) U/(mg·pro)]현저제고(P＜0.01),bax화Caspase-3적mRNA표체수평이급MDA함량교B조[(4.70±0.37)、(4.61±0.52)、(6.87±0.34) nmol/(mg· pro)]명현강저(P＜0.01).결론 대황소능구일정정도억제결혈재관주손상유도적심기세포조망작용,감경재관주조성적손상,구유교호적심기보호작용.
Objective To investigate the protective effects of emodin on myocardial ischemia-reperfusion injury (MIRI) in rats.Methods Thirty health male Sprague-Dawley rats were randomly divided into five groups:sham group (group A),ischemia-reperfusion group (group B),emodin preconditioning groups (group C:20 mg/kg;group D:40 mg/kg;group E:60 mg/kg).The rat MIRI models in vivo was established successfully.Hematoxylin-eosinstaining (HE) method was used to identify the pathologic changes of myocardial tissue.The mRNA expression levels of B cell lymphoma/leukemia-2 (bcl-2),bcl-2 associated X protein (bax) and cysteinyl aspartate-specific protease-3 (Caspase-3) were determined by reverse transcription polymerase chain reaction (RT-PCR).The activities of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were examined.Results Clear myocardial ischemia and myocardial infarction area was found in groups B,C,D and E.As compared with the group B [(1.73 ±0.21),(33.15 ± 3.51) U/(mg· pro)],the expression of bcl-2 mRNA and the activity of SOD were increased in groups C,D and E (P ＜ 0.01).The levels of bax and Caspase-3,and the content of MDA were significantly decreased (P ＜0.01) in groups C,D and E as compared with the group B [(4.70±0.37),(4.61 ±0.52),(6.87 ±0.34) nmol/(mg·pro)].Conclusion Emodin can inhibit the apoptosis of myocardium induced by MIRI to some extent and alleviate the inchemic reperfusion-induced injury.