Traditional Chinese medicine protects against hypertensive kidney injury in Dahl salt-sensitive rats by targeting transforming growth factor-β signaling pathway

Autor: Hongxu Liu, Yuyi Chen, Xing Su, Lumin Qiao, Yixuan Li, Wei Liu, Fuyong Chu, Xingjiang Xiong, Jie Wang
Rok vydání: 2020
Předmět:
0301 basic medicine
Male
medicine.medical_specialty
Bu-Shen-Jiang-Ya decoction (BSJYD)
medicine.medical_treatment
Blood Pressure
Smad Proteins
RM1-950
Kidney
Dahl salt-sensitive (SS) rats
Masson's trichrome stain
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Transforming Growth Factor beta
Internal medicine
Renal fibrosis
medicine
Animals
Medicine
Chinese Traditional
Blood urea nitrogen
Pharmacology
Creatinine
Rats
Inbred Dahl
Chinese medicine
business.industry
Growth factor
Connective Tissue Growth Factor
General Medicine
Rats
CTGF
030104 developmental biology
Endocrinology
chemistry
Valsartan
030220 oncology & carcinogenesis
Hypertension
Kidney Diseases
Therapeutics. Pharmacology
Transforming growth factor-β (TGF-β) signaling pathway
business
Hypertensive kidney injury
medicine.drug
Transforming growth factor
Drugs
Chinese Herbal
Signal Transduction
Zdroj: Biomedicine & Pharmacotherapy, Vol 131, Iss, Pp 110746-(2020)
ISSN: 1950-6007
Popis: This study investigated the therapeutic efficacy of Bu-Shen-Jiang-Ya decoction (BSJYD) on hypertensive renal damage to determine whether it regulates the expression of transforming growth factor-β (TGF-β)/SMADs signaling pathways, thereby relieving renal fibrosis in Dahl salt-sensitive (SS) rats. Dahl SS rats on a high-sodium diet were prospectively treated with BSJYD (n = 12) or valsartan (n = 12) for 8 weeks. The blood pressure (BP) of these rats was measured and their kidneys were subjected to biochemical analysis, including serum creatinine (Scr) and blood urea nitrogen (BUN); hematoxylin and eosin staining; Masson trichrome staining; real-time polymerase chain reaction; and western blot analysis. The primary outcome was that BSJYD significantly reduced BP, debased BUN, and Scr and ameliorated renal pathological changes. As underlying therapeutic mechanisms, BSJYD reduces TGFβ1 and Smad2/3 expression and suppresses renal fibrosis, as suggested by the decreased expression of connective tissue growth factor(CTGF). These data suggest that BSJYD acts as an optimal therapeutic agent for hypertensive renal damage by inhibiting the TGF-β/SMADs signaling pathway.
Databáze: OpenAIRE
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