清润方对糖尿病大鼠肝脏SIRT/NF-κB信号通路的影响

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Abstract Objective To study the effect of Qingrun Formula on sirtuin (SIRT)/nuclear factor-κB (NF-κB) signal pathway in livers of rats with diabetes mellitus and insulin resistance. Methods Ninety 12-week old Wistar male rats were selected as objects, 15 rats were as normal group, the other 75 rats were induced by intraperitoneal injection of Streptozotocin (STZ) and gavage with fat milk for 30 days. After successful modeling, 60 rats with diabetes were randomly divided into model group, Metformin group [250 mg/(kg·d)], high dosage of Qingrun Formula group [11.2 g/(kg·d)], middle dosage of Qingrun Formula group [5.6 g/(kg·d)] and low dosage of Qingrun Formula group [2.8 g/(kg·d)], with 12 rats in each group. Each group was given medicine by gavage, once a day, lasting for 8 weeks. The levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in liver tissues of each group were tested by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expression levels of SIRT1, NF-κB and glucose transporter 4 (GLUT4) in liver tissues of each group were tested by qRT-PCR and Western blot. Results Compared with model group, the level of TNF-α decreased in high dosage of Qingrun Formula group (P ＜ 0.05), the level of IL-6 decreased in high and middle dosage of Qingrun Formula groups (P ＜ 0.05), the mRNA and protein expression levels of SIRT1 increased in each dosage of Qingrun Formula groups (P ＜ 0.05), the mRNA and protein expression levels of GLUT4 increased in high and middle dosage of Qingrun Formula groups (P ＜ 0.05), the mRNA and protein expression levels of NF-κB decreased in the high and middle dosage of Qingrun Formula groups (P ＜ 0.05). Conclusion Qingrun Formula may alleviate the insulin resistance by increasing the expression of SIRT1 and thereby decreasing the expression of NF-κB in the liver of diabetic rats.

Key words： Qingrun Formula Type 2 diabetes mellitus Insulin resistance Sirtuin/nuclear factor-κB signal pathway

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	QIU Zonglin WANG Qiuhong SUN Fenghui WANG Ze LIN Lan▲

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QIU Zonglin WANG Qiuhong SUN Fenghui WANG Ze LIN Lan▲. Effecf of Qingrun Formula on SIRT/NF-κB signal pathway in liver of diabetic rats[J]. 中国医药导报, 2018, 15(28): 4-7,12.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2018/V15/I28/4

[1] 廖涌.中国糖尿病的流行病学现状及展望[J].重庆医科大学学报，2015，40（7）：1042-1045.
[2] 吴家睿.2型糖尿病发生发展的分子机制研究[J].生命科学，2006，18（5）：411-413.
[3] 庞健丽.2型糖尿病三型辨证规范与疗效评价指标的研究[D].北京：中国中医科学院，2009.
[4] 付莹坤，倪青，林兰.清润方对糖尿病大鼠血糖及脂代谢的影响[J].中国中医药信息杂志，2012，19（5）：30-31，35.
[5] Esser N，Paquot N，Scheen AJ. Anti-inflammatory agents to treat or prevent type 2 diabetes，metabolic syndrome and cardiovascular disease [J]. Expert Opin Investig Drugs，2015， 24（3）：283-307.
[6] Odegaard JI，Chawla A. Pleiotropic actions of insulin resistance and inflammation in metabolic homeostasis [J]. Science，2013，339（6116）：172-177.
[7] Baud L，Fouqueray B，Philippe C，et al. Tumor necrosis factor alpha and mesangial cells [J]. Kidney Int，1992，41（3）：600-603.
[8] Firneisz G. Non-alcoholic fatty liver disease and type 2 diabetes mellitus：the liver disease of our age?[J]. World J Gastroenterol，2014，20（27）：9072-9089.
[9] Watson RT，Pessin JE. Intracellular organization of insulin signaling and GLUT4 translocation [J]. Recent Prog Horm Res，2001，56：175-193.
[10] Senn JJ，Klover PJ，Nowak IA，et al. Interleukin-6 induces cellular insulin resistance in hepatocytes [J]. Diabetes，2002，51（12）：3391-3399.
[11] 常化静，吴新荣，何羡霞，等.IKK/NF-KB信号通路与2型糖尿病及中药抗炎治疗[C]//广东省药学会.2014年广东省药师周大会论文集，2017：209-213.
[12] Guarani V，Deflorian G，Franco CA，et al. Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase [J]. Nature，2011，473（7346）：234-238.
[13] Jeon BT，Kim KE，Heo RW，et al. Myeloid-specific deletion of SIRT1 increases hepatic steatosis and hypothalamic inflammation in mice fed a high-fat diet [J]. Metab Brain Dis，2014，29（3）：635-643.
[14] Cao Y，Jiang X，Ma H，et al. SIRT1 and insulin resistance [J]. J Diabetes Complications，2016，30（1）：178-183.
[15] Gilbert RE，Thai K，Advani SL，et al. SIRT1 activation ameliorates hyperglycaemia by inducing a torpor-like state in an obese mouse model of type 2 diabetes [J]. Diabetologia，2015，58（4）：819-827.
[16] Rosebeck S，Madden L，Jin X，et al. Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-κB activation [J]. Science，2011，331（6016）：468-472.
[17] Dandona P，Aljada A，Chaudhuri A，et al. Metabolic syndrome: a comprehensive perspective based on interactions between obesity，diabetes，and inflammation [J]. Circulation，2005，111（11）：1448-1454.
[18] Wang S，Zhao Y，Xia N，et al. KPNβ1 promotes palmitate-induced insulin resistance via NF-κB signaling in hepatocytes [J]. J Physiol Biochem，2015，71（4）：763-772.
[19] Wei Y，Gao J，Qin L，et al. Tanshinone Ⅰ alleviates insulin resistance in type 2 diabetes mellitus rats through IRS-1 pathway [J]. Biomed Pharmacother，2017，93：352-358.
[20] Shinozaki S，Chang K，Sakai M，et al. Inflammatory stimuli induce inhibitory S-nitrosylation of the deacetylase SIRT1 to increase acetylation and activation of p53 and p65 [J]. Sci Signal，2014，7（351）：ra106.