活血化痰方对非酒精性脂肪肝大鼠模型的实验研究
摘要
目的：
通过复制非酒精性脂肪肝(NAFLD)大鼠模型并予以活血化痰方干预,探讨非酒精性脂肪肝可能的发病机制,探讨活血化痰方对NAFLD大鼠模型的干预、治疗的可能机制,为临床应用活血化痰方防治NAFLD提供实验依据。
方法：
健康雄性SD大鼠60只,体重130-150g,级别为清洁级,适应性饲养一周后,按体重编号,完全随机分为正常组(A组,10只)和高脂造模组60只。高脂饲料饲组又分为模型组(B组,20只),二甲双胍干预组(C组,10只),活血化痰方低剂量干预组(D组,10只),活血化痰方高剂量干预组(E组,10只)。自饲养第8周起,模型组每周随机处死1只大鼠,取肝脏HE染色确定B组大鼠达到重度脂肪肝后结束实验。实验过程中观察大鼠的一般情况,HE染色对肝脏脂肪变性程度及炎症程度进行分级、评分,全自动生化分析仪检测血清中ALT、AST、TG、TC含量,免疫蛋白印迹检测法检测模型组及空白组大鼠肝组织中CBS、CSE蛋白水平的表达,检测血清、肝组织NO、 H2S水平,采用酶联免疫吸附法(ELISA)测定血清瘦素、脂联素、IL-6、IL-10、TNF-α水平。
结果：
1.本实验16周成功复制了大鼠重度非酒精性脂肪性肝(NAFLD)模型。16周末时模型组大鼠体重明显高于正常组,(P<0.01),B组大鼠肝重量明显高于A组(P<0.05),B组大鼠肝指数明显高于A组(P<0.01),与正常组相比,模型组大鼠血清ALT、AST、TG、TC水平明显升(P<0.05或P<0.01),与A组相比,B组大鼠肝脏脂肪变程度显著增加(P<0.01),与A组相比,B组大鼠肝脏炎症程度显著增加(P<0.01),与A组比较,B组大鼠肝脏肝组织NO的含量明显增加,H2S含量明显减少,两组有显著性差异(P<0.01),大鼠肝组织中CBS、CSE蛋白表达水平结果,B组与A组比较,CBS, CSE蛋白表达水平明显减低,两组均有显著性差异(P<0.05)。与A组相比,B组大鼠血清NO水平明显升高(P<0.01),与A组相比,B组大鼠血清H2S水平明显降低(P<0.05),与A组相比,B组大鼠血清IL-6水平明显升高(P<0.01),与A组相比,B组大鼠血清TNF-α水平明显升高(P<0.05),与A组相比,B组大鼠血清IL-6水平明显升高(P<0.01),与A组相比,B组大鼠血清TNF-α水平明显升高(P<0.05)；与A组相比,B组大鼠血清瘦素含量明显升高(P<0.01),脂联素含量明显降低(P<0.05)。
2.C、D、E组大鼠腹腔脂肪组织较模型组含量少,肝脏体积稍大,偏黄色或暗红色,部分大鼠肝脏切面有油腻感。B组大鼠肝组织可见重度弥漫性肝细胞大泡性脂肪变,C、D、E组大鼠轻、中度肝细胞大泡性脂肪变,较模型组减轻,A组大鼠肝脏无明显炎性改变,B组肝脏炎性改变较明显,大量肝细胞肿胀伴有气球样变,部分小叶内有少量坏死灶,汇管区可见大量炎性细胞浸润并且向小叶内延伸,小部分有炎性细胞聚集,C、D、E组大鼠少量肝细胞肿胀伴气球样变,无明显小叶内有坏死灶,汇管区少许炎性细胞浸润,偶有有炎性细胞聚集,较B组明显减轻。
3.与A组大鼠相比,B组肝组织中CBS、CSE蛋白表达水平显著降低(P<0.05)；与B组相比,C、D、E组蛋白表达水平增高(P<0.05,或P<0.01),与C组相比,D、E组均无差异,D、E组之间无差异。与A组大鼠相比,B组肝组织中NO显著增高(P<0.01),与B组相比,C、D、E干预组肝组织中NO降低(P<0.05,或P<0.01),与C组相比,D、E干预组之间均无差异；与A组相比,B组肝组织中H2S降低(P<0.01),与B组相比,C、D、E组肝组织中H2S升高(P<0.05,或P<0.01),与C、D、E组均无差异,D、E组之间无差异；
4.与A组大鼠相比,B组血清中ALT、AST、TG、TC显著增高(P<0.01)；与B相比,C、D、E组血清中ALT、AST、TG、TC显著降低(P<0.05,或P<0.01)；与C组相比,D、E组均无差异,D、E组之间无差异。
5.与A组大鼠相比,B血清中瘦素水平显著升高(P<0.01)；与B组相比,C组、D组、E组血清中瘦素显著降低(P<0.05,或P<0.01)；与C组相比,E组无差异；与D组有显著差异；与A组大鼠相比,B组血清中脂联素水平显著降低(P<0.01)；与B组相比,C组、D组、E组血清中脂联素水平显著升高(P<0.05,或P<0.01)；与C组相比,D组、E组无差异；D组、E组之间无差异
6.血清中IL-6、IL-10、TNF-α的含量变化；血清IL-6水平与A组大鼠相比,B组显著升高,C组、D组、E组较模型组降低,但三者之间无明显差异；与A组比较,B组血清IL-10水平显著降低(P<0.01)；与B组相比,C组、D组、E组血清中IL-10水平显著提高(P<0.05,或P<0.01),C组、E组较活D组提高显著；血清TNF-a水平与A组比较,B及D组显著增高(P<0.01),C组、E剂量组较B组有显著降低；
结论：
1.高脂饲料喂养8周成功复制了大鼠单纯性脂肪肝(NAFL),16周功复制了大鼠重度非酒精性脂肪性肝炎(NASH)模型；
2.活血化痰方有减少非酒精性脂肪性肝病大鼠血清TG、TC含量,有降低ALT、AST作用,可有效干预非酒精性脂肪性肝病大鼠模型的形成；减少血清中IL-6、TNF-α的生成,促进血清中IL-10的生成,可明显减轻非酒精性脂肪性肝病中的炎症反应；
3.脂联素、瘦素在脂肪肝的发病过程中起了重要作用,活血化痰方提高大鼠血清中脂联素、降低瘦素含量,防治非酒精性脂肪肝；
4.高脂饲养脂肪肝的发病机制可能与H2S的生成有关,活血化痰方可明显提高CBS、CSE蛋白表达水平,调高血清中H2S浓度,延缓脂肪肝的进程。
Objective:
Copy of nonalcoholic fatty liver disease (NAFLD) rat model and to intervene to explore the pathogenesis of non-alcoholic fatty liver may explore Huoxue side of NAFLD rat model of intervention, treatment and possible mechanisms, the clinical application Huoxue prescription preventing NAFLD to provide experimental basis.
Methods:
Healthy male SD rats of60, weight130-150g level for the clean-level, adaptive feeding after a week, according to the weight number, completely randomly divided into normal group (group A,10) and fat-made module60. High fat diet fed group was divided into model group (group B,20), metformin intervention group (C10), blood circulation and resolving side low dose of the intervention group (Group D,10), the high side of Huoxue dose in the intervention group (group E,10).8weeks feeding, the model group weekly random one rat were sacrificed, liver HE staining to determine the end of the experiment group B rats with severe fatty liver. General situation observed in rats in the experiment, HE staining of liver steatosis and inflammation grade score, automatic biochemical analyzer to detect the serum of ALT, AST, TG, TC content, Western blot assay detection model CBS, in the liver tissue of the treated group, expression of CSE protein levels in serum, liver tissue NO level of H2S, using enzyme-linked immunosorbent assay (ELISA), serum leptin, adiponectin, IL-6, IL-10, TNF-alpha level.
Results:
1、In this study,16weeks successfully copied the rats with severe non-alcoholic fatty liver (NAFLD) model.16weekend, the body weight of rats of model group was significantly higher than the normal group (P<0.01), group B in rat liver weight was significantly higher than group A (P<0.05), group B rat liver index was significantly higher than group A (P<0.01), Group B rats fasting blood glucose was significantly higher than group A (P<0.05)60min A and B group blood glucose was significantly increased fasting blood glucose of group B was significantly higher than group A (P<0.01)120min A and B, two sets of blood glucose began to decrease, but the group B rats, fasting blood glucose was significantly higher than group A (P<0.01), compared with the normal group, model group, serum ALT, AST, and TG TC levels were significantly rose (P<0.05or P<0.01), compared with group A, group B in rat liver steatosis increased significantly (P<0.01), compared with group A, group B in rat liver the degree of inflammation was significantly increased (P<0.01) compared with group A, group B in rat liver liver tissue content of NO significantly increased significantly reduce the H2S content of the two groups have significant difference (P<0.01), CBS, in the liver tissue of CSE The protein levels of the results of group B and group A, CBS, of CSE protein expression levels were significantly reduced in both groups there were significant differences (P<0.05). Compared with group A, B, serum NO level was significantly increased (P<0.01), compared with group A, B serum H2S levels were significantly lower (P<0.05), compared with group A, B, serum IL-6levels were significantly increased (P<0.01), compared with group A, group B rats serum TNF-α levels were significantly increased (P<0.05) compared with group A, group B mouse serum IL-6levels were significantly increased (P<0.01) compared with group A, group B serum levels of TNF-a levels were significantly increased (P<0.05); Compared with group A, B serum leptin were significantly lower (P<0.01), adiponectin was significantly increased (P<0.05).
2、C, D and E in rat peritoneal adipose tissue compared with the model group content, the liver volume is slightly larger, partial yellow or dark red, part of the rat liver slice greasy feeling. Group B of rat liver tissue visible macrovesicular steatosis in severe diffuse liver cells, rats in group C and D, E, light, moderate hepatocyte macrovesicular steatosis, compared with model group, group A in rat liver without obvious inflammation changes, group B hepatic inflammatory changes more significantly, a large number of liver cell swelling with ballooning degeneration, a small amount of some intralobular necrosis, portal area shows inflammatory cell infiltration and extends to the intralobular small part of the inflammatory cells aggregation, swelling of the rats in group C, D and E, a small number of liver cells with ballooning degeneration, no significant lobular necrosis, portal area a little inflammatory cell infiltration, and occasional inflammatory cell aggregation, compared with group B was significantly reduced.
3、Compared with group A, group B in liver tissue, CBS, of CSE protein expression levels were significantly lower (P<0.05); Compared with group B, C, D and Group E protein expression level increased (P<0.05,P<0.01), compared with group C, D, E, no difference, D, group E, no difference. Compared with rats in group A, group B liver tissues, NO was significantly increased (P<0.01) compared with group B, C and D and E in the intervention group liver tissue NO lower (P<0.05or P<0.01) There was no difference between compared with group C, D, E, in the intervention group; compared with group A, group B liver tissue of H2S lower (P<0.01) compared with group B, C and D, E, liver organization of H2S increased (P<0.05or P<0.01), and C, D, E, no difference, D, group E, no difference;
4、Compared with group A, group B, serum ALT and AST, TG and TC were significantly higher (P<0.01); compared with B, C, D and Group E in serum ALT and AST, TG and the TC was significantly decreased (P<0.05or P <0.01); compared with group C, D and E group was no difference, D, E, with no difference between
5、Compared with group A, B, serum leptin levels were significantly higher (P<0.01); compared with Group B, Group C, Group D, Group E in serum leptin was significantly lower (P<0.05, or P<0.01); compared with group C, E group no difference; and D groups were significantly different; compared with rats in group A, B serum adiponectin levels were significantly lower (P <0.01); and B group compared to group C, group D, E, serum adiponectin levels were significantly increased (P<0.05or P<0.01); compared with group C and group D, group E no difference; group D, E no differences between the groups
6、In serum IL-6, IL-10, TNF-alpha content changes; serum IL-6levels compared with rats in group A, group B was significantly higher in group C and Group D, E group than in model group However, no significant difference between the three; compared with group A, B serum level of IL-10significantly reduced (P<0.01); compared with group B, group C, group D, group E in serum IL-10levels significantly increased (P<0.05or P<0.01), C, group, group E compared with living in group D to improve significantly; serum of TNF-alpha levels of group A, B, and D group significantly with increased (P<0.01), and C, group E dose group than in group B had a significantly lower;
Conclusion:
1、High fat diet8weeks successfully copied the rat simple fatty liver disease (of NAFL),16weeks successfully copied the model of rats with severe non-alcoholic steatohepatitis (NASH);
2、Huoxue side to reduce non-alcoholic fatty liver disease serum TG, TC content, reduce the ALT, AST role of effective interventions for non-alcoholic fatty liver disease rat model of formation; a decrease of serum IL-6, TNF-alpha generation, and promote the generation of serum IL-10can significantly reduce the inflammatory response in non-alcoholic fatty liver disease;
3、Adiponectin and leptin in the pathogenesis of fatty liver played an important role in blood circulation and resolving side increase in serum adiponectin and lower leptin levels, prevention and treatment of non-alcoholic fatty liver;
4、High-fat diet fatty liver pathogenesis may be related to the formation of H2S in related Huoxue be significantly improved CBS, of CSE protein expression levels, an increase in serum concentration of H2S, delaying the process of fatty liver.
通过复制非酒精性脂肪肝(NAFLD)大鼠模型并予以活血化痰方干预,探讨非酒精性脂肪肝可能的发病机制,探讨活血化痰方对NAFLD大鼠模型的干预、治疗的可能机制,为临床应用活血化痰方防治NAFLD提供实验依据。
方法：
健康雄性SD大鼠60只,体重130-150g,级别为清洁级,适应性饲养一周后,按体重编号,完全随机分为正常组(A组,10只)和高脂造模组60只。高脂饲料饲组又分为模型组(B组,20只),二甲双胍干预组(C组,10只),活血化痰方低剂量干预组(D组,10只),活血化痰方高剂量干预组(E组,10只)。自饲养第8周起,模型组每周随机处死1只大鼠,取肝脏HE染色确定B组大鼠达到重度脂肪肝后结束实验。实验过程中观察大鼠的一般情况,HE染色对肝脏脂肪变性程度及炎症程度进行分级、评分,全自动生化分析仪检测血清中ALT、AST、TG、TC含量,免疫蛋白印迹检测法检测模型组及空白组大鼠肝组织中CBS、CSE蛋白水平的表达,检测血清、肝组织NO、 H2S水平,采用酶联免疫吸附法(ELISA)测定血清瘦素、脂联素、IL-6、IL-10、TNF-α水平。
结果：
1.本实验16周成功复制了大鼠重度非酒精性脂肪性肝(NAFLD)模型。16周末时模型组大鼠体重明显高于正常组,(P<0.01),B组大鼠肝重量明显高于A组(P<0.05),B组大鼠肝指数明显高于A组(P<0.01),与正常组相比,模型组大鼠血清ALT、AST、TG、TC水平明显升(P<0.05或P<0.01),与A组相比,B组大鼠肝脏脂肪变程度显著增加(P<0.01),与A组相比,B组大鼠肝脏炎症程度显著增加(P<0.01),与A组比较,B组大鼠肝脏肝组织NO的含量明显增加,H2S含量明显减少,两组有显著性差异(P<0.01),大鼠肝组织中CBS、CSE蛋白表达水平结果,B组与A组比较,CBS, CSE蛋白表达水平明显减低,两组均有显著性差异(P<0.05)。与A组相比,B组大鼠血清NO水平明显升高(P<0.01),与A组相比,B组大鼠血清H2S水平明显降低(P<0.05),与A组相比,B组大鼠血清IL-6水平明显升高(P<0.01),与A组相比,B组大鼠血清TNF-α水平明显升高(P<0.05),与A组相比,B组大鼠血清IL-6水平明显升高(P<0.01),与A组相比,B组大鼠血清TNF-α水平明显升高(P<0.05)；与A组相比,B组大鼠血清瘦素含量明显升高(P<0.01),脂联素含量明显降低(P<0.05)。
2.C、D、E组大鼠腹腔脂肪组织较模型组含量少,肝脏体积稍大,偏黄色或暗红色,部分大鼠肝脏切面有油腻感。B组大鼠肝组织可见重度弥漫性肝细胞大泡性脂肪变,C、D、E组大鼠轻、中度肝细胞大泡性脂肪变,较模型组减轻,A组大鼠肝脏无明显炎性改变,B组肝脏炎性改变较明显,大量肝细胞肿胀伴有气球样变,部分小叶内有少量坏死灶,汇管区可见大量炎性细胞浸润并且向小叶内延伸,小部分有炎性细胞聚集,C、D、E组大鼠少量肝细胞肿胀伴气球样变,无明显小叶内有坏死灶,汇管区少许炎性细胞浸润,偶有有炎性细胞聚集,较B组明显减轻。
3.与A组大鼠相比,B组肝组织中CBS、CSE蛋白表达水平显著降低(P<0.05)；与B组相比,C、D、E组蛋白表达水平增高(P<0.05,或P<0.01),与C组相比,D、E组均无差异,D、E组之间无差异。与A组大鼠相比,B组肝组织中NO显著增高(P<0.01),与B组相比,C、D、E干预组肝组织中NO降低(P<0.05,或P<0.01),与C组相比,D、E干预组之间均无差异；与A组相比,B组肝组织中H2S降低(P<0.01),与B组相比,C、D、E组肝组织中H2S升高(P<0.05,或P<0.01),与C、D、E组均无差异,D、E组之间无差异；
4.与A组大鼠相比,B组血清中ALT、AST、TG、TC显著增高(P<0.01)；与B相比,C、D、E组血清中ALT、AST、TG、TC显著降低(P<0.05,或P<0.01)；与C组相比,D、E组均无差异,D、E组之间无差异。
5.与A组大鼠相比,B血清中瘦素水平显著升高(P<0.01)；与B组相比,C组、D组、E组血清中瘦素显著降低(P<0.05,或P<0.01)；与C组相比,E组无差异；与D组有显著差异；与A组大鼠相比,B组血清中脂联素水平显著降低(P<0.01)；与B组相比,C组、D组、E组血清中脂联素水平显著升高(P<0.05,或P<0.01)；与C组相比,D组、E组无差异；D组、E组之间无差异
6.血清中IL-6、IL-10、TNF-α的含量变化；血清IL-6水平与A组大鼠相比,B组显著升高,C组、D组、E组较模型组降低,但三者之间无明显差异；与A组比较,B组血清IL-10水平显著降低(P<0.01)；与B组相比,C组、D组、E组血清中IL-10水平显著提高(P<0.05,或P<0.01),C组、E组较活D组提高显著；血清TNF-a水平与A组比较,B及D组显著增高(P<0.01),C组、E剂量组较B组有显著降低；
结论：
1.高脂饲料喂养8周成功复制了大鼠单纯性脂肪肝(NAFL),16周功复制了大鼠重度非酒精性脂肪性肝炎(NASH)模型；
2.活血化痰方有减少非酒精性脂肪性肝病大鼠血清TG、TC含量,有降低ALT、AST作用,可有效干预非酒精性脂肪性肝病大鼠模型的形成；减少血清中IL-6、TNF-α的生成,促进血清中IL-10的生成,可明显减轻非酒精性脂肪性肝病中的炎症反应；
3.脂联素、瘦素在脂肪肝的发病过程中起了重要作用,活血化痰方提高大鼠血清中脂联素、降低瘦素含量,防治非酒精性脂肪肝；
4.高脂饲养脂肪肝的发病机制可能与H2S的生成有关,活血化痰方可明显提高CBS、CSE蛋白表达水平,调高血清中H2S浓度,延缓脂肪肝的进程。
Objective:
Copy of nonalcoholic fatty liver disease (NAFLD) rat model and to intervene to explore the pathogenesis of non-alcoholic fatty liver may explore Huoxue side of NAFLD rat model of intervention, treatment and possible mechanisms, the clinical application Huoxue prescription preventing NAFLD to provide experimental basis.
Methods:
Healthy male SD rats of60, weight130-150g level for the clean-level, adaptive feeding after a week, according to the weight number, completely randomly divided into normal group (group A,10) and fat-made module60. High fat diet fed group was divided into model group (group B,20), metformin intervention group (C10), blood circulation and resolving side low dose of the intervention group (Group D,10), the high side of Huoxue dose in the intervention group (group E,10).8weeks feeding, the model group weekly random one rat were sacrificed, liver HE staining to determine the end of the experiment group B rats with severe fatty liver. General situation observed in rats in the experiment, HE staining of liver steatosis and inflammation grade score, automatic biochemical analyzer to detect the serum of ALT, AST, TG, TC content, Western blot assay detection model CBS, in the liver tissue of the treated group, expression of CSE protein levels in serum, liver tissue NO level of H2S, using enzyme-linked immunosorbent assay (ELISA), serum leptin, adiponectin, IL-6, IL-10, TNF-alpha level.
Results:
1、In this study,16weeks successfully copied the rats with severe non-alcoholic fatty liver (NAFLD) model.16weekend, the body weight of rats of model group was significantly higher than the normal group (P<0.01), group B in rat liver weight was significantly higher than group A (P<0.05), group B rat liver index was significantly higher than group A (P<0.01), Group B rats fasting blood glucose was significantly higher than group A (P<0.05)60min A and B group blood glucose was significantly increased fasting blood glucose of group B was significantly higher than group A (P<0.01)120min A and B, two sets of blood glucose began to decrease, but the group B rats, fasting blood glucose was significantly higher than group A (P<0.01), compared with the normal group, model group, serum ALT, AST, and TG TC levels were significantly rose (P<0.05or P<0.01), compared with group A, group B in rat liver steatosis increased significantly (P<0.01), compared with group A, group B in rat liver the degree of inflammation was significantly increased (P<0.01) compared with group A, group B in rat liver liver tissue content of NO significantly increased significantly reduce the H2S content of the two groups have significant difference (P<0.01), CBS, in the liver tissue of CSE The protein levels of the results of group B and group A, CBS, of CSE protein expression levels were significantly reduced in both groups there were significant differences (P<0.05). Compared with group A, B, serum NO level was significantly increased (P<0.01), compared with group A, B serum H2S levels were significantly lower (P<0.05), compared with group A, B, serum IL-6levels were significantly increased (P<0.01), compared with group A, group B rats serum TNF-α levels were significantly increased (P<0.05) compared with group A, group B mouse serum IL-6levels were significantly increased (P<0.01) compared with group A, group B serum levels of TNF-a levels were significantly increased (P<0.05); Compared with group A, B serum leptin were significantly lower (P<0.01), adiponectin was significantly increased (P<0.05).
2、C, D and E in rat peritoneal adipose tissue compared with the model group content, the liver volume is slightly larger, partial yellow or dark red, part of the rat liver slice greasy feeling. Group B of rat liver tissue visible macrovesicular steatosis in severe diffuse liver cells, rats in group C and D, E, light, moderate hepatocyte macrovesicular steatosis, compared with model group, group A in rat liver without obvious inflammation changes, group B hepatic inflammatory changes more significantly, a large number of liver cell swelling with ballooning degeneration, a small amount of some intralobular necrosis, portal area shows inflammatory cell infiltration and extends to the intralobular small part of the inflammatory cells aggregation, swelling of the rats in group C, D and E, a small number of liver cells with ballooning degeneration, no significant lobular necrosis, portal area a little inflammatory cell infiltration, and occasional inflammatory cell aggregation, compared with group B was significantly reduced.
3、Compared with group A, group B in liver tissue, CBS, of CSE protein expression levels were significantly lower (P<0.05); Compared with group B, C, D and Group E protein expression level increased (P<0.05,P<0.01), compared with group C, D, E, no difference, D, group E, no difference. Compared with rats in group A, group B liver tissues, NO was significantly increased (P<0.01) compared with group B, C and D and E in the intervention group liver tissue NO lower (P<0.05or P<0.01) There was no difference between compared with group C, D, E, in the intervention group; compared with group A, group B liver tissue of H2S lower (P<0.01) compared with group B, C and D, E, liver organization of H2S increased (P<0.05or P<0.01), and C, D, E, no difference, D, group E, no difference;
4、Compared with group A, group B, serum ALT and AST, TG and TC were significantly higher (P<0.01); compared with B, C, D and Group E in serum ALT and AST, TG and the TC was significantly decreased (P<0.05or P <0.01); compared with group C, D and E group was no difference, D, E, with no difference between
5、Compared with group A, B, serum leptin levels were significantly higher (P<0.01); compared with Group B, Group C, Group D, Group E in serum leptin was significantly lower (P<0.05, or P<0.01); compared with group C, E group no difference; and D groups were significantly different; compared with rats in group A, B serum adiponectin levels were significantly lower (P <0.01); and B group compared to group C, group D, E, serum adiponectin levels were significantly increased (P<0.05or P<0.01); compared with group C and group D, group E no difference; group D, E no differences between the groups
6、In serum IL-6, IL-10, TNF-alpha content changes; serum IL-6levels compared with rats in group A, group B was significantly higher in group C and Group D, E group than in model group However, no significant difference between the three; compared with group A, B serum level of IL-10significantly reduced (P<0.01); compared with group B, group C, group D, group E in serum IL-10levels significantly increased (P<0.05or P<0.01), C, group, group E compared with living in group D to improve significantly; serum of TNF-alpha levels of group A, B, and D group significantly with increased (P<0.01), and C, group E dose group than in group B had a significantly lower;
Conclusion:
1、High fat diet8weeks successfully copied the rat simple fatty liver disease (of NAFL),16weeks successfully copied the model of rats with severe non-alcoholic steatohepatitis (NASH);
2、Huoxue side to reduce non-alcoholic fatty liver disease serum TG, TC content, reduce the ALT, AST role of effective interventions for non-alcoholic fatty liver disease rat model of formation; a decrease of serum IL-6, TNF-alpha generation, and promote the generation of serum IL-10can significantly reduce the inflammatory response in non-alcoholic fatty liver disease;
3、Adiponectin and leptin in the pathogenesis of fatty liver played an important role in blood circulation and resolving side increase in serum adiponectin and lower leptin levels, prevention and treatment of non-alcoholic fatty liver;
4、High-fat diet fatty liver pathogenesis may be related to the formation of H2S in related Huoxue be significantly improved CBS, of CSE protein expression levels, an increase in serum concentration of H2S, delaying the process of fatty liver.
引文
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