The protective effect of Jinlida granules on kidney of type 1 diabetic rats / 第二军医大学学报

ABSTRACT

Objective To explore the protective effect of Jinlida granuleson kidney tissues of type 1 diabetic rats, and to elucidate the related mechanism. Methods SD rats were intraperitoneally injected with streptozotocin (STZ, 60 mg/kg) to establish type 1 diabetic models. Then the model rats were randomly divided into diabetic model group, low-, medium- and high-dose Jinlida groups (0. 75, 1. 5 and 3. 0 g/kg Jinlida granules, respectively), Jinlida + Tongxinluo (TXL) group (1. 5 g/kg Jinlida granules+ 0. 4 g/kg TXL), metformin group (50 mg/kg metformin), and saxagliptin group (1 mg/kg saxagliptin), with each group containing 5 rats. Five healthy rats served as normal controls. Eight weeks after administration of drugs or placebo, the levels of growth hormone (GH), growth hormone receptor (GHR), insulin-like growth factor 1 (IGF-1), insulin-like growth factor 1 receptor (IGF-1R), and insulin-like growth factor lbinding protein 1 (IGFBP-1) mRNA were detected by real-time quantitative PCR, the expressions of MAPK pathway related proteins and fibronectin (FN) were determined by Western blotting; and H-E staining, Masson staining and PAS staining were used to observe the morphological changes of kidney tissues. Results Compared with the normal control group, the levels of GH, GHR, IGF-1, IGF-1R mRNA and the protein expressions of p-ERK, p-JNK, and FN of kidney tissues were significantly increased (P<0. 01), with cellular proliferation and fibrous deposition seen in the kidney tissues in the diabetic model group. After intervention with midde and high-dose Jinhda granules, the levels of GH, GHR, IGF-1, and IGF-1R mRNA and ratios of p-ERK/ERK, p-JNK/JNK, and FN protein expression were significantly decreased (P<0. 05, P<0. 01), with alleviated kidney tissues fibrosis. Conclusion Jinlida granules can protett kidney tissues of type 1 diabetic rats, which is probably through up-regulating the levels of GH and IGF-l mRNA and inhibiting the activation of the MAPK pathway.