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Dendrobium candidum protects against diabetic kidney lesions through regulating vascular endothelial growth factor, Glucose Transporter 1, and connective tissue growth factor expression in rats
Author(s) -
Chang Jingzhi,
Zhou Yuanting,
Cong Guobin,
Guo Hui,
Guo Yali,
Lu Kun,
Li Yi chuan,
Tian Hua
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28666
Subject(s) - ctgf , endocrinology , medicine , diabetic nephropathy , vascular endothelial growth factor , diabetes mellitus , kidney , growth factor , streptozotocin , creatinine , glucose transporter , renal cortex , connective tissue , dendrobium , insulin , receptor , pathology , vegf receptors , traditional medicine
Diabetes mellitus (DM) remains a great health problem with approximate 30% of patients with DM eventually suffering from diabetic nephropathy. The search for exogenous protective factors has recently received wide attention. The current study aimed to investigate the protective effects of Dendrobium candidum (DC) on kidneys in diabetic rats. Initially, streptozotocin‐induced diabetic rats were established and randomly divided into the model group, DC group (0.2, 0.4, and 0.8 g/kg) and irbesartan group (17.5 mg/kg). The biochemical indexes, pathological changes, and the expressions of vascular endothelial growth factor (VEGF), GLUT‐1, and CTGF were examined. It was found that as compared with the model group, the kidney index, serum creatine, blood urea nitrogen, 24‐hour urine protein, and VEGF of DC treatment groups were significantly decreased, and pathological changes in kidney were improved in the DC groups and irbesartan group ( P < 0.05 for each parameter). The protein and messenger RNA levels of GLUT‐1 and CTGF in treatment groups were significantly lower than those in rats' renal cortex without treatment. Our data suggest that DC may protect the kidneys of diabetic rats via regulating expression of VEGF, GLUT‐1, and CTGF.