Effect of Guanxin Danshen Formulation on diabetic kidney disease in db/db mice through regulation of Nrf2 pathway.
10.19540/j.cnki.cjcmm.20200418.401
- Author:
Bin ZHANG
1
;
Xue-Lian ZHANG
1
;
Chen-Yang ZHANG
1
;
Gui-Bo SUN
1
;
Xiao-Bo SUN
1
Author Information
1. Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences Beijing 100193, China Key Laboratory of New Drug Discovery based on Classic Chinese Medicine Prescription, Chinese Academy of Medical Sciences Beijing 100193, China Key Laboratory of Efficacy Evaluation of Chinese Medicine against Glycolipid Metabolic Disorders, State Administration of Traditional Chinese Medicine Beijing 100193, China.
- Publication Type:Journal Article
- Keywords:
Guanxin Danshen Formulation;
diabetes mellitus;
diabetic kidney disease(DKD);
estrogen receptor;
oxidative stress
- MeSH:
Animals;
Creatinine;
Diabetes Mellitus;
Diabetic Nephropathies;
Kidney;
Kidney Glomerulus;
Mice;
NF-E2-Related Factor 2;
Salvia miltiorrhiza
- From:
China Journal of Chinese Materia Medica
2020;45(11):2595-2600
- CountryChina
- Language:Chinese
-
Abstract:
Diabetic kidney disease(DKD) has become a primary cause of end-stage kidney disease, without any effective treatment available. In this study, we assessed the protective effect of Guanxin Danshen Formulation(GXDSF) on diabetic nephropathy in db/db mice. The db/m and db/db mice were randomly divided into 4 groups: control group, model group, metformin group, and GXDSF group. After 8 weeks' treatment with GXDSF, metformin or normal saline, the mice were sacrificed, and the blood and kidney tissues were collected for the further analysis. Compared with the model group, TG, TCH and LDL levels significantly decreased in the GXDSF group. The results from HE and PAS staining showed that db/db mice exhibited abnormal kidney tissues with increased glomerular volume, basement-membrane thickening and mesangial cell proliferation, which could be significantly alleviated by GXDSF treatment. GXDSF treatment also reduced serum creatinine and BUN. Meanwhile, GXDSF treatment markedly elevated GSH-PX levels, while reduced LDH and MDA levels in the kidney tissues. Western blot assay showed that GXDSF evidently up-regulated protein levels of ERα and p-Akt, and subsequently promoted HO-1 expression mediated by Nrf2. These data collectively indicated that GXDSF protects db/db mice against DN by regulating ERα and Nrf2-mediated HO-1 expression.
