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[目的]观察疏肝祛瘀通络降浊法对非酒精性脂肪性肝炎(NASH)大鼠肝组织髓样分化蛋白-2(MD-2)和诱导型一氧化氮合酶(iNOS)基因表达的影响,以探讨二者在NASH发病中的作用。[方法]雄性SD大鼠分为模型组,疏肝祛瘀通络降浊法低剂量(低剂量)组、中剂量组、高剂量组,阳性对照组,预防组和正常组,除正常组外,其余各组大鼠以高脂饮食喂养4周后用不同剂量的中药和阳性对照药灌胃治疗,12周后全部处死。同期设正常饮食组作为对照。免疫组织化学方法观察肝组织核转录因子-κB(NF-κB)表达,逆转录聚合酶链反应(RT-PCR)法观察肝组织MD-2和iNOS mRNA的表达。[结果]12周时,中剂量组大鼠肝组织NF-κB表达较模型组下调;肝组织MD-2mRNA(0.132±0.058)和iNOS mRNA(0.164±0.061)表达较模型组(0.795±0.294和1.029±0.388)减弱(均P<0.01)。[结论]大鼠NASH形成后,肝组织MD-2和iNOS mRNA的表达上调,可能与二者参与了NASH大鼠内毒素性肝损伤有关。疏肝祛瘀通络降浊法可以通过减轻内毒素性肝损伤下调NASH大鼠肝组织MD-2和iNOSmRNA的表达。
[Objective] To observe the effect of Shugan Quyu Tongluo Jiangzhuo on the expression of MD-2 and inducible nitric oxide synthase (iNOS) genes in non-alcoholic steatohepatitis (NASH) rats Expression in order to explore the role of the two in the pathogenesis of NASH. [Methods] Male Sprague-Dawley rats were divided into model group, low dose (low dose) group, middle dose group, high dose group, positive control group, prophylaxis group and normal group except Shugan Quyu Tongluo Jiangzhuo method except normal group In addition, the rats in other groups were fed with high-fat diet for 4 weeks, then treated with different doses of traditional Chinese medicine and positive control, and were sacrificed 12 weeks later. The same period set the normal diet group as a control. Immunohistochemistry was used to observe the expression of nuclear factor-κB (NF-κB) in liver tissue and the expression of MD-2 and iNOS mRNA in liver tissue by reverse transcription-polymerase chain reaction (RT-PCR) [Results] At 12 weeks, the expression of NF-κB in liver tissue was decreased in the middle-dose group compared with the model group. The expression of MD-2 mRNA (0.132 ± 0.058) and iNOS mRNA (0.164 ± 0.061) 1.029 ± 0.388) (all P <0.01). [Conclusion] The up-regulation of MD-2 and iNOS mRNA expression in rat liver after NASH formation may be related to their involvement in endotoxic liver injury in NASH rats. Shugan Quyu Tongluo Jiangzhuo method can reduce the expression of MD-2 and iNOSmRNA in liver tissue of NASH rats by reducing endotoxin-induced hepatic injury.