摘要
目的观察虫草菌丝对实验性大鼠非酒精性脂肪肝(NAFLD)的治疗效果,探讨其可能的分子机制。方法高脂饮食建立大鼠NAFLD模型,同时设正常饮食对照组(Basic diet,B组),模型对照组(单纯性非酒精性脂肪肝组,NAFL组),病理对照组(非酒精性脂肪性肝炎组,NASH组),虫草菌丝治疗组(CS组)。HE染色法观察肝脏病理改变;ELISA测定血清TNFα;免疫组织化学染色观察肝组织TNFα,解耦联蛋白2(UCP2)表达情况;逆转录PCR检测肝组织UCP2mRNA;鲎试剂法测血清内毒素。结果(1)NAFL组肝组织广泛脂肪变性,脂质沉积;UCP2表达增加,而TNFα、血清内毒素水平均无显著变化;(2)NASH组肝组织广泛弥漫脂肪变性,炎性细胞浸润、坏死,局部纤维组织增生;UCP2、TNFα、血清内毒素水平均显著升高;(3)CS组肝组织广泛脂肪变性,仅有轻微炎性细胞浸润,未见坏死灶及纤维组织增生;UCP2、TNFα、血清内毒素水平均显著下降。结论早期UCP2表达上调,可能是机体的适应性反应,而晚期UCP2过度表达、TNFα水平升高以及内毒素血症共同诱导或加剧脂肪性肝病向脂肪性肝炎,甚至向脂肪性肝纤维化发展。虫草菌丝能发挥有效的护肝作用,可能通过上调UCP2,减轻内毒素血症,下调TNFα等多靶点、多途径发挥治疗作用。
Objective To explore the effect of Cordyceps sinensis （cs）on high-fat diet induced nonalcoholic fatty liver diseases （NAFLD） in experimental rats and its possible molecular mechanisms. Methods Thirty-two SD rats were randomly divided into basic diet-treated group（B group）,model group（M group）.pathology group（P group） and CS treated group（G group）, Liver histopathologic evaluation erformed by hermatoxylin-eosin staining. Serum tumor necrosis factor alpha（TNFα） level was performed by enzyme-linked immunoadsordent assay（ELISA）. Ucp2 and TNFα proteins expression in hepatocytes was examined by immunohistochemistry.and UCP2mRNA expression by semi-quantitatlve reverse transcription-polymerasc chain reaction （RT- PCR）. The level of serum exdotoxin was determined by limulus lysate test. Results （ 1 ）Compared with B group, no evident increase was found in the level of serum TNFα and endotoxin of M group rats. Neither marked change in number of hepatocytes with TNFαpositive was shown by immunohistochemistry staining, but an increase in UCP2 mRNA and UCP2 protein expression was seen in M group rats. （2） Compared with M group, a significant increase in serum TNFα and endotoxin levels was found in P group. An apparent increase in number of hepatocytes with TNFα and UCP2 positive was shown by immunohistochemistry staining. as well as UCP2mRNA level by RT-PCR. （3） Compared with P group, a significant decrease in serum TNFα and endotoxin levels was found in G group. A little lower level of UCP2 expression was shown in G group than in P group. Conclusion High level of serum and tissue TNFα, serum endotoxin and UCP2 over-expression induce or exacerbate fatty liver disease progression to steatohepatitis even fibrosis. CS could inhibit steatohepatitis derived from NAFLD by reversing them.
出处
《重庆医学》
CAS
CSCD
2006年第18期1671-1673,共3页
Chongqing medicine
关键词
非酒精性脂肪肝
解耦联蛋白2
肿瘤坏死因子Α
内毒素血症
虫草菌丝
nonalcoholic farty liver
uncoupling protein-2
serum tumor necrosis factor alpha （TNFα）
serum endotoxin=cordyceps sinensis （cs）
