非酒精性脂肪性肝炎(NASH)是非酒精性脂肪性肝病一个病理阶段，是病情进展的关键环节，直接关系到疾病预后，但临床上仍缺乏有效的治疗手段。因此，本研究在前期证实"脂肝方"对NASH有效基础上，从NASH脂肪酸氧化应激、线粒体损伤，ATP减少导致肝细胞炎症与死亡的关键环节出发，运用电镜观察肝细胞线粒体、自噬体等超微结构；ELISA检测血清丙二醛、β-羟化壬烯，游离脂肪酸、AMP激活的蛋白激酶、细胞色素C；Western blot检测凋亡相关因子Bcl-2、caspase3及NF-κB/p65、TNF-α表达，免疫组化法检测胀亡、自噬特征性蛋白p62、PARP、Beclin1；HPLC检测血清ATP含量，从而通过"FFA-线粒体-ATP/NF-κB-TNF-α"通路障碍导致肝细胞炎症及凋亡、胀亡与自噬的途径，为揭示NASH的分子机制，"肝病实脾"理论科学内涵及脂肝方对NASH防治的效应机制。

Non-alcoholic steatohepatitis (NASH) is a pathological stage of non-alcoholic fatty liver disease (NAFLD), and it is also the key segments of the progress of this disease, which is directly related to disease ending, but it is still a lack of effective clinical treatment.Therefore, on the basis of the "Zhiganfang" effectively to NASH in the past study，this study confirmed in fatty acid oxidative stress, mitochondrial damage, ATP reduced , that cause liver cell inflammation and death in NASH,by electron microscopy to observe liver cell mitochondria, autophagic body ultrastructure; and ELISA for detection of serum malondialdehyde, beta-hydroxylation of nonene, free fatty acids, AMP-activated protein kinase, cytochrome C; and Western blot detecting NF-κB/p65; Immuno- histochemical method detecting apoptosis-related factors Bcl-2, caspase3 and inflammation-related factors, TNF-α protein expression, and oncosis, autophagic protein p62, PARP, Beclin1 ; HPLC detecting serum ATP , so as to FFA- mitochondrial-ATP/NF-κB-TNF-α " pathway obstacles cause liver cell inflammation and apoptosis, oncosis and autophagy pathway, we will reveal the molecular mechanism of NASH, and theoretical science connotation to "liver disease cured by enhanced Spleen" and effective mechanism of "Zhiganfang" to prevention and treatment of NASH.