Effect of Jiangzhi granules on expression of leptin receptor mRNA, P-JAK2 and P-STAT3 in rats with non-alcoholic fatty liver disease
- Author:
- No author available
- Journal Title:
- WORLD CHINESE JOURNAL OF DIGESTOLOGY
- Issue:
- 32
- DOI:
- 10.3969/j.issn.1009-3079.2007.32.003
- Key Word:
- 降脂颗粒;东宝甘泰;非酒精性脂肪肝;Leptin;瘦素受体mRNA;P-JAK2;P-STAT3
Abstract： 目的:观察降脂颗粒对非酒精性脂肪肝大鼠的治疗作用及其对血清瘦素、肝组织瘦素受体mRNA、P-JAK2/P-STAT3蛋白含量表达的影响.方法:将60只SD♂大鼠,随机分为空白组(正常饮食)和造模组(高脂饮食).待造模成功后将造模组大鼠随机分为模型对照组、降脂颗粒低、中、高剂量组和东宝甘泰组.治疗4 wk后行肝组织生化和病理学检测,并同时应用ELISA试剂盒检测血清瘦素,RT-PCR法检测肝组织瘦素受体mRNA表达,应用Western blot检测肝组织P-JAK2和P-STAT3蛋白的表达.结果:低、中、高剂量组降脂颗粒能明显降低非酒精性脂肪肝大鼠模型肝脂(TG和TC)水平,改善脂肪变性,降低肝脏炎症反应,并能明显降低血清瘦素高水平状态(193.02±23.8 ng/L,163.97±31.38 ng/L,147.83±17.59 ng/L vs 317.22±39.26 ng/L,P＜0.01),改善瘦素抵抗,同时增加瘦素受体mRNA的表达(1.87±0.06,2.20±0.04,2.78±0.04 vs 1.50±0.05,P＜0.01),增加肝组织P-JAK2和P-STAT3蛋白的含量(119.88±2.98,123.45±0.68,124.34±3.42 vs 113.15±1.27,P＜0.01;94.15±0.78,100.18±3.33,101.94±2.20 vs 89.06±0.69,P＜0.01).结论:降脂颗粒对非酒精性脂肪肝大鼠肝脏脂质和炎症有较好的治疗作用,其可能机制是改善瘦素抵抗,增加肝脏瘦素受体mRNA表达及P-JAK2,P-STAT3蛋白含量.
- [1]赵彩彦,李丽,李建梅,等.非酒精性脂肪性肝病大鼠肝组织瘦素受体表达的变化[J].2005,(6).
- [2]赵文霞,段荣章,苗明三,等.赤芍对大鼠脂肪肝模型胰岛素抵抗及瘦素影响的实验研究[J].2005,(9).
- [3]王泰龄,刘霞,周元平.慢性肝炎炎症活动度及纤维化程度计分方案[J].1998,(4).
- [4]Robert G. Knodell,Kamal G. Ishak,William C. Black,etc.Formulation and application of a numerical scoring system for assessing histological activity in asymptomatic chronic active hepatitis[J].1981,1(5).
- [5]钟岚,范建高,王国良,等.肥胖、高脂血症性脂肪性肝炎模型的建立[J].2000,(2).
- [6]Edward D, Javor,Marc G, Ghany,Elaine K, Cochran,etc.Leptin reverses nonalcoholic steatohepatitis in patients with severe lipodystrophy.[J].2005,41(4).
- [7]Balasubramaniyan V,Nalini N.Effect of hyperleptinaemia on chronic ethanol-induced hepatotoxicity in mice.[J].2006,20(2).
- [8]曾民德.脂肪肝[J].1999,(2).
- [9]Koteish A,Diehl AM.Animal models of steatosis.[J].2001,21(1).
- [10]K Tobe,T Ogura,C Tsukamoto,etc.Relationship between serum leptin and fatty liver in Japanese male adolescent university students[J].1999,94(11).
- [11]Nicolson M,Bennett L,Burgess TL,etc.Altered cell surface expression and signaling of leptin receptors containing the fatty mutation.[J].1998,273(29).
- [12]Plata Salaman-CR,Flynn MC.Leptin (OB protein) and meal size (editorial)[J].1999,15(6).
- [13]Elmstahl S,Berglund G,Ahren B,etc.Evidence for leptin regulation of food intake in humans.[J].1998,83(12).
- [14]Symes A,Karow ML,Carpenter LR,etc.Enhancing leptin response by preventing SH2-containing phosphatase 2 interaction with Ob receptor.[J].1998,95(11).
- [15]Kubota N,Ohsumi J,Nagai R,etc.Increased expression of the sterol regulatory element-binding protein-1 gene in insulin receptor substrate-2(-/-) mouse liver.[J].2001,276(42).
- [16]Diehl A.M.,Goodman Z.,Ishak K.G..Alcohollike liver disease in nonalcoholics[J].1988.
- [17]Petersen KF,Oral EA,Dufour S,etc.Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy.[J].2002,109(10).
- [18]Richardet JP,Bories PN,Campillo B,etc.Serum leptin levels in alcoholic liver cirrhosis: relationship with gender, nutritional status, liver function and energy metabolism.[J].2001,55(11).
- [19]Natale S,Brizi M,Bianchi G,etc.Nonalcoholic fatty liver disease: a feature of the metabolic syndrome.[J].2001,50(8).
- [20]J, Bartek,J, Bartos,J, Galuska,etc.Expression of ob gene coding the production of the hormone leptin in hepatocytes of liver with steatosis.[J].2001,145(1).