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tangnaikang improves insulin resistance and β-cell apoptosis by ameliorating metabolic inflammation in ***-Lepr^(cp)/NDmcr rats

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Journal of Traditional Chinese Medicine 2017年第3期37卷 361-370页

作者： Li Linyi Hisae Yoshitomi Qin Lingling Wu Xinli Zhou Tian Wang Haiyan Jiang Yueying Wei Ying Xu Tunhai Liu Tonghua Gao Ming Health-cultivation Laboratory of the Ministry of Education Beijing University of Chinese Medicine Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases Beijing Institute of Heart Lung and Blood Vessel Diseases Beijing Anzhen Hospital Capital Medical University School of Pharmaceutical Sciences Mukogawa Women's University Oncology Department Dongfang Hospital Beijing University of Chinese Medicine

OBJECTIVE: To investigate the effects of tangnaikang(TNK), a mixture of five herbal plant extracts,on inflammation-mediated insulin resistance andβ-cell apoptosis in ***-Leprcp/NDmcr(SHR-cp)***: Seven-week-old SHR-cp rats were randomly divided into a control(CON) group and a TNK(3.24 g/kg) group. Wistar-Kyoto rats at the same age were used as the normal control *** 7 weeks of continuous intragastric administration of TNK, the glucose metabolic status and insulin sensitivity of the rats were evaluated by assessing fasting serum glucose(FBG), the oral glucose tolerance test(OGTT), fasting serum insulin(FINS),and the insulin sensitivity index(ISI). Serum tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), C-reactive protein(CRP) and adiponectin were measured via enzyme-linked immunosorbent *** infiltration and apoptosis in adipose tissues were detected through F4/80 immunohistochemistry and the terminal deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. Islet morphology and β-cell apoptosis were investigated using double immunofluorescence staining and the TUNEL assay. The expression of cytokine genes in adipose tissue, the liver, and the pancreas was detected in real-time polymerase chain reaction assays. The expression and phosphorylation levels of insulin signaling-, inflammation-, and β-cell survival-related proteins in the liver and pancreas of SHR-cp rats were detected by western ***: TNK(3.24 g/kg) treatment significantly decreased body weight, FBG and FINS; improved impaired glucose tolerance; increased the ISI; reduced serum levels of TNF-α, CRP and IL-6; and increased serum adiponectin. The m RNA expression of inflammatory markers was markedly reduced in the liver, pancreas, and adipose tissue. F4/80-and TUNEL-positive cells in adipose tissues were decreased, as was the number of TUNEL-positiveβ-cells. The phosphorylation of c-Jun N-terminal kinase and that of insulin receptor substrate-1 at seri

关键词： Metabolic inflammation Insulin resis-tance Islets of langerhans Apoptosis Rats, inbredSHR tangnaikang

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Effect of tangnaikang on TGF-β_1-induced transdifferentiation of human renal tubular epithelial HK-2 cells

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Journal of Traditional Chinese Medicine 2013年第3期33卷 388-393页

作者： Lixia Yang Xinhuan Ma Tao Cheng Tonghua Liu Lili Wu Wen Sun Margetts Peter Joseph Central Laboratory of Gansu Province Academy of Traditional Chinese Medicine Pharmacy Department Gansu Province Hospital of Traditional Chinese Medicine Institute of Traditional Chinese Medicine Information Gansu Province Academy of Traditional Chinese Medicine Science and Technology Department Beijing University of Traditional Chinese Medicine Department of Nephrology St. Joseph's Hospital of McMaster University

OBJECTIVE： To explore the function of Tangnai- kang （TNK） in the prevention and treatment of re- nal interstitial fibrosis through transdifferentiation of the human renal tubular epithelial cell line HK-2 induced bytransforming growth factor-β1 （TGF-β1）. METHODS： HK-2 cells cultured in dulbecco＇s modi- fied eagle medium/F12 （1：1） with 10% fetal calf se- rum were divided into six groups： blank control group, TGF-β1 group （TGF-β1 10 ng/mL）, serum con- trol group （TGF-β1 10 ng/mL ＋ 10% serum）, treat- ment group 1 （TGF-β1 10 ng/mL ＋ 5% TNK serum）, treatment group 2 （TGF-β1 10 ng/mL＋10% TNK se-rum）, and treatment group 3 （TGF-β1 10 ng/mL＋ 20% TNK serum）. Cell proliferation was detected by 4,5-Dimethylthiazol-2-yl）-2,5-diphenyltetrazoliu m bromide assay. Expression of a-smooth muscle ac- tin （a-SMA） and E-cadherin were observed by im- munohistochemical assay. The contents of collagen Ⅰ （Col Ⅰ）, collagen Ⅲ（ColⅢ）, and fibronectin （FN） in the culture medium supernatant were detected by ELISA. RESULTS： E-cadherin was expressed and α-SMA was not expressed in normal HK-2 cells. In HK-2 cells cultured with TGF-β1, α-SMA expression signifi- cantly increased, HK-2 cells significantly proliferat- ed, and secretion of Col Ⅰ, Col Ⅲ, and FN significantly increased compared with the blank control group （all P〈0.05）. In the HK-2 cells cultured with TGF-β1 and TNK serum, the expression of α-SMA signifi- cantly decreased, the expression of E-cadherin sig- nificantly increased, and the cell proliferation and the secretion of Col Ⅰ, Col Ⅲ and FN were significant- ly inhibited compared with the TGF-β1 group （all P〈 0.05. CONCLUSION： TNK can inhibit cell proliferation and reduce secretion of Col Ⅰ, Col Ⅲ, and *** in- dicates that TNK can inhibit transdifferentiation of human renal tubular epithelial cells induced by TGF-β1, with the effect of preventing and treating renal interstitial fibrosis.

关键词： Transforming growth factor beta 1 Epi-thelial cells Cell proliferation Cell Transdifferentia-tion tangnaikang

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