摘要
目的探讨纳洛酮对大鼠酒精性脂肪肝的作用及其可能机制。方法48只Wistar雄性大鼠按随机数字表法分为酒精性脂肪肝模型组、低剂量药物组、高剂量药物组和正常对照组。第4周末，处死所有大鼠，分别检测血液和组织中超氧化物歧化酶（SODJ、丙二醛（MDA）和β-内啡肽（β-EP）含量，同时用免疫组织化学方法检测β-EP和肿瘤坏死因子α（（TNF—α）在肝组织中的分布，并行肝脏病理组织学检查。结果与模型组相比，其他3组MDA和β-EP含量明显降低（均P〈0．01），β-EP阳性细胞数和TNF—α阳性细胞数明显减少（均P〈0．01），SOD含量明显上升（均P〈0．01），且3组比较，差异也有统计学意义（均P〈0.01）；病理检查发现处理组肝脏脂肪变程度明显减轻。免疫组织化学染色发现β-EP阳性细胞和TNF-α阳性细胞在肝内的数量和分布与脂肪变性程度和区域一致。结论纳洛酮可通过降低血浆和组织中β-EP水平，升高血浆和组织中SOD含量，抗脂质过氧化而有效防治酒精性脂肪肝形成，且呈量效关系。
Objective To investigate the effect of naloxone on alcoholic fatty liver （AFL） in rats and its possible mechanism. Methods Forty-eight Wistar male rats were divided randomly into four groups： fatty liver group （n=12）, low naloxone group （n=12）, high naloxone group （n=12） and control group （n=12）. By the end of the 4th week all rats were sacrificed and the liver sample was taken. The plasma and tissue levels of β-EP, superoxidized dismutase （SOD） and malondialdehyde （MDA） were measured. Histopathological ancl immunohistochemical examinations of liver tissue were performed. Results Compared with those in fatty liver group, the plasma levels of SOD in low and high naloxone groups increased, while MDA and -EP decreased （P〈0.01）. The degree of hepaticyte fatty degeneration in low and high naloxone groups was markedly alleviated and was close to that of control group. The amounts and distribution areas of β-EP and TNF-α positive cells were consistent with the degree and distribution areas of formation of alcoholic fatty liver by decreasing plasma fatty degenerative hepatic cells. Conclusion Naloxone can prevent the β--endorphin and anti-lipid peroxide oxidation
出处
《浙江医学》
CAS
2009年第7期933-935,共3页
Zhejiang Medical Journal
关键词
纳洛酮
酒精性脂肪肝
Β-内啡肽
肿瘤坏死因子Α
Naloxone Alcoholic fatty liver（AFL） β-endorphin（β-EP） Tumor necrosis factor a （TNF- a）
