Effect of Kangxianling Decoction on Expression of TGF-β1/Smads and Extracellular Matrix Deposition. (1st January 2019)

• Record Type: Journal Article
• Authors: Ji, Jing; He, Liqun
• Other Names: Du Caigan Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2019(2019)
• Publication Date: 2019-01-01
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2019/5813549
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Kangxianling (KXL) decoction is a traditional Chinese herbal formulation which has been used to treat early and midterm chronic renal failure. Renal fibrosis is a common characteristic of progressive chronic kidney diseases (CKD). The formation of renal fibrosis is caused by kidney trauma, infection, and immune response. The pathophysiological mechanism of renal fibrosis was mainly due to increased collagen synthesis in the kidney, decreased degradation, and a large amount of extracellular matrix (ECM) deposition. The purpose of this study was intended to evaluate the effect of Kangxianling decoction on expression of TGF- β 1/Smad signaling pathway in renal fibrosis rats. 50 specific pathogen-free Sprague Dawley (SPF SD) rats were randomly divided into five groups: control group, sham group, 5/6 nephrectomy model group, 5/6 nephrectomy model plus KXL decoction (21g /kg) group, and 5/6 nephrectomy model plus Losartan Potassium (LP) (33.3 g/kg) group. The rats were all sacrificed after two months and the left kidney tissue was sampled. HE staining was used to observe the renal pathological changes and the score of kidney damage was made. Masson staining was used to observe the degree of renal fibrosis. Immunohistochemical staining, western blot, and qRT-PCR were used to detect the expression levels of related molecules in TGF- β 1/Smad signaling pathway. The results suggested that KXL could lighten renal histopathology damage, downregulate the expression of TGF- β 1 (transforming growth factor- β 1), Smad2/3, CTGF (connective tissue growth factor), Collagen I, and Collagen III, and upregulate the expression level of Smad7.