Tripterygium wilfordii mitigates hyperglycemia-induced upregulated Wnt/β-catenin expression and kidney injury in diabetic rats
Autor: | Lei Liu, Baochao Chang, Yan Zhang, Weidong Chen, Ping Yang |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cancer Research medicine.medical_specialty nuclear factor-κB 030204 cardiovascular system & hematology Diabetic nephropathy 03 medical and health sciences 0302 clinical medicine Irbesartan Immunology and Microbiology (miscellaneous) GSK-3 Diabetes mellitus Internal medicine medicine transforming growth factor-β1 Kidney Oncogene biology business.industry diabetic nephropathy General Medicine Articles β-catenin medicine.disease biology.organism_classification Streptozotocin 030104 developmental biology medicine.anatomical_structure Endocrinology glycogen synthase kinase 3β Wnt-1 Tripterygium wilfordii business medicine.drug |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-1015 1792-0981 |
Popis: | Aberrant activation of the Wnt/β-catenin pathway contributes to the development of diabetic nephropathy (DN); however, treatment with Tripterygium wilfordii (TW) may be beneficial for patients with DN. The aim of the present study was to evaluate the effect of TW on Wnt/β-catenin expression in the kidneys of diabetic rats. Male Sprague-Dawley rats were randomly injected with vehicle (control) or streptozotocin to induce diabetes. Diabetic rats were then randomly treated with vehicle (sodium carboxymethyl cellulose; SCC), TW combined with SCC (8 or 16 mg/kg) or irbesartan (50 mg/kg) daily for 8 weeks. Metabolic parameter levels and renal pathological changes were examined. mRNA and protein expression of Wnt-1, glycogen synthase kinase (GSK)-3β, β-catenin, nuclear factor (NF)-κB and transforming growth factor (TGF)-β1 in the kidneys of rats from all groups were measured. Compared with the DM group, metabolic parameters and morphological parameters, apart from blood glucose levels, were significantly improved in TW-treated rats (all P |
Databáze: | OpenAIRE |
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