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目的探讨高密度脂蛋白(HDL)对严重烧伤大鼠心功能的保护作用。方法将135只Wistar大鼠随机分为对照组、烧伤组和实验组。对照组15只大鼠,不作任何处理;烧伤组和实验组各60只大鼠,均于背部造成30%TBSAⅢ度烫伤(以下称烧伤)创面,实验组伤后立即经尾静脉注入HDL(80mg/kg),伤后30min两组大鼠经腹腔补充平衡盐溶液(50ml/kg).检测对照组及两组烧伤大鼠伤后12、24、48、72h血清肌酸激酶(CK)、细胞间黏附分子(ICAM)1及肿瘤坏死因子(TNF)α的含量;观察对照组及其他两组大鼠伤后48h心肌组织病理学变化。结果与烧伤组比较,实验组大鼠CK、ICAM-1及TNF-α含量均降低,下降率分别为36.5%、32.0%、12.6%(P<0.05或0.01);对照组CK、ICAM-1及TNF-α含量明显低于烧伤组(P<0.01).对照组心肌纤维大小均匀、线粒体结构清楚;与烧伤组比较,实验组伤后48h心肌细胞变性、炎性细胞浸润及线粒体肿胀程度减轻,且未见细胞溶解坏死。结论HDL对严重烧伤大鼠心功能的保护作用,可能与抑制ICAM-1、TNF-α、CK的表达有关。
Objective To investigate the protective effect of high density lipoprotein (HDL) on cardiac function in severely burned rats. Methods 135 Wistar rats were randomly divided into control group, burn group and experimental group. Fifty rats in the control group were treated with no treatment. The rats in the burn group and the experimental group each received 30% TBSA Ⅲ degree scald wounds on their backs. The wounds in the experimental group were injected with HDL (80mg / kg), and 30 minutes after the injury, the rats in both groups were given the balanced salt solution (50ml / kg) intraperitoneally.Serum creatine kinase (CK), 12, 24, 48 and 72 h after injury were detected in the control group and the two groups of burn rats, (ICAM) 1 and tumor necrosis factor (TNF) α were measured. The myocardial histopathological changes of the control group and the other two groups were observed 48 h after injury. Results Compared with the burn group, the contents of CK, ICAM-1 and TNF-α in the experimental group were decreased, the decreasing rates were 36.5%, 32.0% and 12.6% (P <0.05 or 0.01) (P <0.01) .The myocardial fiber in the control group was uniform in size and the structure of mitochondria was clear. Compared with the burn group, the myocardial cell degeneration, inflammatory cell infiltration and mitochondria swelling in the experimental group were alleviated at 48h , And no cell lysis necrosis. Conclusion The protective effects of HDL on heart function in severely burned rats may be related to the inhibition of the expression of ICAM-1, TNF-α and CK.