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Tangnaikang improves insulin resistance and β-cell apoptosis by ameliorating metabolic inflammation in SHR.Cg-Leprcp/NDmcr rats

Author: Li LY, Hisae Y, Qin LL, Wu XL, Zhou T, Wang HY, Jiang YY, Wei Y, Xu TH, Liu TH, Gao M
Page: 361

OBJECTIVE: To investigate the effects of Tangnaikang (TNK), a mixture of five herbal plant extracts, on inflammation-mediated insulin resistance and B-cell apoptosis in SHR.Cg-Leprcp/NDmcr (SHR-cp) rats. METHODS: 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 group. After 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-a (TNF-a), interleukin-6 (IL-6), C-reactive protein (CRP) and adiponectin were measured via enzyme-linked immunosorbent assays. Macrophage infiltration and apoptosis in adipose tissues were detected through F4/80 immunohistochemistry and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Islet morphology and B-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 B-cell survival-related proteins in the liver and pancreas of SHR-cp rats were detected by western blotting. RESULTS: 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-a, CRP and IL-6; and increased serum adiponectin. The mRNA 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-positive B-cells. The phosphorylation of c-Jun N-terminal kinase and that of insulin receptor substrate-1 at serines 307 and 1101 was significantly decreased. In the pancreas, the expression of nuclear factor kappa-light chain-enhancer of activated B cells-p65 was significantly decreased, and phosphoinositide 3-kinase and IRS-2 were significantly increased. CONCLUSION: TNK was able to improve insulin resistance and B-cell apoptosis in SHR-cp rats, which might be associated with its ability to relieve the overall and local metabolic inflammatory responses observed in SHR-cp rats.

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