辨证治疗对非酒精性脂肪性肝病大鼠脂质过氧化及病理的影响

目的：探讨中医辨证治疗对非酒精性脂肪性肝病（NAFLD）大鼠肝脏脂质过氧化及病理影响。方法：取SPF级Wistar。大鼠72只，雌雄各半，随机分为正常组、模型组、对照药物治疗组、药物A方治疗组、药物B方治疗组，先A方后B方治疗组、先B方后A方治疗组、先空白后A方治疗组、先空白后B方治疗组，共9组。除正常组给予普通饲料外，其余各组大鼠饲以高脂饲料。造模第4周后，模型组加用等体积生理盐水灌胃；对照组加用对照药物灌胃；药物A方组加用治疗药物A方灌胃；药物B方组加用治疗药物B方灌胃；先A方后B方治疗组即4～8周用A方，8～12周用B方灌胃；先B方后A方治疗组即4～8周用B方，8～12周用A方灌胃；先空白后A方治疗组即先空白，第8～12周用A方灌胃；先空白后B方治疗组即先空白，第8～12周用B方灌胃。实验第12周时，测定大鼠肝组织SOD、MDA、GSH—ST的含量及评定大鼠肝组织脂肪变性程度及病理炎症活动度。结果：实验第12周时，先A方后B方治疗组提高NAFLD后期大鼠的肝组织SOD、GSH—ST含量的疗效与其他治疗组相比尤为显著（P〈0．01），降低脂质过氧化产物MDA含量的疗效显著（P〈0．01或尸〈0．05）；在对肝脏病理影响方面，先A方后B方治疗组减轻NAFLD后期大鼠肝细胞脂肪变，降低炎症活动度的疗效明显（P〈0．05或P〈0．01）。结论：在NAFLD的整个病程中，采取早期阶段运用疏肝健脾、活血化瘀、化痰利湿的治法，后期阶段运用化痰消瘀、清热利湿、补益肝肾治法的治疗方案，对于提高大鼠脂肪肝细胞抗氧化能力，降低脂质过氧化产物，减轻大鼠肝细胞脂肪变、降低炎症活动度的疗效显著优于其他治疗措施。

Influence of traditional Chinese medicine on liver lipid per-oxidation and pathology in NAFLD rats

Objective： To explore the of traditional Chinese medicine on liver lipid per-oxidation and pathology in nonalcoholic fatty liver disease （NAFLD） rats. Methods： Fetched 72 wistar rats＇ level of SPF, females and males were half and half, were divided into 9 groups at random： normal group, model group, comparison medicine treatment group, medicine A treatment group, medicine B treatment group, first Medicine A then medicine B treatment group, first medicine B then medicine A treatment group, first blank then medicine A treatment group, first blank then , medicine B treatment group. Except the normal group was fed ordinary diet, the other eight groups were fed by high fat and high cholesterol diet. After 4 weeks later, model group rats were given hpysiological saline by intragastric administration. Comparison medicine treatment group rats were given comparision medicine by intragastric administration. Medicine A treatment group rats were given medicine A by intragastric administration. Medicine B treatment group rats were given medicine B by intragastric administration. First medicine A then medicine B treatment group rats were given medicine A from 4 weeks to 8 weeks and medicine B from 8 weeks to 12 weeks by intragastric administration. First medicine B then medicine A treatment group rats were given medicine B from 4 weeks to 8 weeks and medicine A from 8 weeks to 12 weeks by intragastric administration. First blank then medicine A treatment group rats were given nothing from 4 weeks to 8 weeks and medicine A from 8 weeks to 12 weeks by intragastric administration. First blank then medicine B treatment group rats were given nothing from 4 weeks to 8 weeks and medicine B from 8 weeks to 12 weeks by intragastricadministration. At the end of the 12 weeks, we determined the content of SOD, MDA and GSH-ST and evaluated the degree of fat denatured and the activity of pathology inflammation in rat liver organization. Results： At the end of the 12 weeks, first medicine A then medicine B treatment group had b