Biochanin-A has antidiabetic, antihyperlipidemic, antioxidant, and protective effects on diabetic nephropathy via suppression of TGF-β1 and PAR-2 genes expression in kidney tissues of STZ-induced diabetic rats.


Journal

Biotechnology and applied biochemistry
ISSN: 1470-8744
Titre abrégé: Biotechnol Appl Biochem
Pays: United States
ID NLM: 8609465

Informations de publication

Date de publication:
Oct 2022
Historique:
received: 12 05 2021
accepted: 03 10 2021
pubmed: 16 10 2021
medline: 1 11 2022
entrez: 15 10 2021
Statut: ppublish

Résumé

One of the major complications of diabetes is diabetic nephropathy, and often many patients suffer from diabetic nephropathy. That is why it is important to find the mechanisms that cause nephropathy and its treatment. This study was designed to examine the antidiabetic effects of biochanin A (BCA) and evaluate its effects on oxidative stress markers and the expression of transforming growth factor-β1 (TGF-β1) and protease-activated receptors-2 (PAR-2) genes in the kidney of type 1 diabetic rats. After induction of diabetes using streptozotocin (STZ), 55 mg/kg bw dose, rats were randomly divided into four groups with six rats in each group as follows: normal group: normal control receiving normal saline and a single dose of citrate buffer daily; diabetic control group: diabetic control receiving 0.5% dimethyl sulfoxide daily; diabetic+BCA (10 mg/kg) group: diabetic rats receiving biochanin A at a dose of 10 mg/kg bw daily; diabetic+BCA (15 mg/kg) group: diabetic rats receiving biochanin A at a dose of 15 mg/kg bw daily. TGF-β1 and PAR-2 gene expression was assessed by real-time. Spectrophotometric methods were used to measure biochemical factors: fast blood glucose (FBG), urea, creatinine, albumin, lipids profiles malondialdehyde (MDA), and superoxide dismutase (SOD). The course of treatment in this study was 42 days. The results showed that in the diabetic control group, FBG, serum urea, creatinine, expression of TGF-β1 and PAR-2 genes, and the levels of MDA in kidney tissue significantly increased and SOD activity in kidney tissue and serum albumin significantly decreased compared to the normal group (p < 0.001). The results showed that administration of biochanin A (10 and 15 mg/kg) after 42 days significantly reduced the expression of TGF-β1 and PAR-2 genes and FBG, urea, creatinine in serum compared to the diabetic control group (p < 0.001), also significantly increased serum albumin compared to the diabetic control group (p < 0.001). The level of MDA and SOD activity in the tissues of diabetic rats that used biochanin A (10 and 15 mg/kg) was significantly reduced and increased, respectively, compared to the diabetic control group (p < 0.001). Also, the result showed that in the diabetic control group lipids profiles significantly is disturbed compared to the normal group (p < 0.001), the results also showed that biochanin A (10 and 15 mg/kg) administration could significantly improved the lipids profile compared to the control diabetic group (p < 0.001). It is noteworthy that it was found that the beneficial effects of the biochanin A were dose dependent. In conclusion, administration of biochanin A for 42 days has beneficial effect and improves diabetes and nephropathy in diabetic rats. So probably biochanin A can be used as an adjunct therapy in the treatment of diabetes.

Identifiants

pubmed: 34652037
doi: 10.1002/bab.2272
doi:

Substances chimiques

Streptozocin 5W494URQ81
Transforming Growth Factor beta1 0
Antioxidants 0
biochanin A U13J6U390T
Hypoglycemic Agents 0
Creatinine AYI8EX34EU
Hypolipidemic Agents 0
Receptor, PAR-2 0
Superoxide Dismutase EC 1.15.1.1
Serum Albumin 0
Lipids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2112-2121

Informations de copyright

© 2021 International Union of Biochemistry and Molecular Biology, Inc.

Références

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Auteurs

Jamal Amri (J)

Traditional and Complementary Medicine Research Center, Department of Traditional medicine, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Mona Alaee (M)

Traditional and Complementary Medicine Research Center, Department of Traditional medicine, School of Medicine, Arak University of Medical Sciences, Arak, Iran.
Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Rasool Babaei (R)

Traditional and Complementary Medicine Research Center, Department of Traditional medicine, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Zahra Salemi (Z)

Department of Biochemistry and Genetics, Arak University of Medical Sciences, Arak, Iran.

Reza Meshkani (R)

Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Ali Ghazavi (A)

Department of Immunology & Microbiology, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Ahmad Akbari (A)

Traditional and Complementary Medicine Research Center, Department of Traditional medicine, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

Mehdi Salehi (M)

Traditional and Complementary Medicine Research Center, Department of Traditional medicine, School of Medicine, Arak University of Medical Sciences, Arak, Iran.

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