ReferenceID 4798

Kaempferol inhibits renal fibrosis by suppression of the sonic hedgehog signaling pathway

Phytomedicine

Background: Most chronic kidney diseases (CKDs) develop to end-stage renal disease (ESRD), which is characterized by fibrosis and permanent tissue and function loss. As a result, better and more effective remedies are es

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Reference Id
4798
Evidence Id
21388
Core Evidence Id
21388
Source Reference Id
2847
Herb2 Reference Id
HBREF003644
Subject Paper Key
HBIN019495_36274411
Pubmed Id
36274411
Doi
10.1016/j.phymed.2022.154246
Paper Title
Kaempferol inhibits renal fibrosis by suppression of the sonic hedgehog signaling pathway
Paper Abstract
Background: Most chronic kidney diseases (CKDs) develop to end-stage renal disease (ESRD), which is characterized by fibrosis and permanent tissue and function loss. As a result, better and more effective remedies are essential. Kaempferol (KAE) is a common flavonoid extracted from plants. It can control the progression of kidney fibrosis and the epithelial-to-mesenchymal transition (EMT) of the renal tubular system. Purpose: We aim to investigate the effect of KAE therapy on extracellular matrix deposition and stimulation of EMT in vitro and in vivo to elucidate the treatment mechanisms regulating these effects. Study design: Chronic hypertension-induced kidney fibrosis was studied in spontaneously hypertensive rats with chronic kidney disease. Biochemical analysis, histological staining, and the expression level of relative proteins were used to assess the effect of KAE on renal function and fibrosis. The direct impact of KAE on proliferation and migration was evaluated using human renal tubular epithelial cells (HK-2) induced by transforming growth factor-β1 (TGF-β1), which can then induce EMT. The molecular mechanism of KAE was verified using co-IP assay and immunofluorescence. Results: KAE could reduce blood pressure and decrease the extracellular matrix (ECM) components (including collagen I and collagen Ш), TGF-β1, and α-SMA in the kidneys of hypertension-induced rats with chronic kidney disease. Moreover, in HK-2 cell treated with TGF-β1, KAE administration significantly suppressed proliferation, migration, and EMT via increasing the expression of E-cadherin, while reducing the N-cadherin and α-SMA. Sufu was exceedingly repressed in HK-2 cells treated with TGF-β1. KAE inhibited the activation of Shh and Gli through increasing the expression of Sufu, thereby blocking the nuclear translocation of Gli1 in vitro. Conclusion: KAE ameliorated kidney fibrosis and EMT by inhibiting the sonic hedgehog signaling pathway, thereby to attenuate the pathological progression of hypertensive kidney fibrosis.
Journal
Phytomedicine
Publish Year
2022
Experiment Subject
rat; human; hk-2 cell; hk-2 cells
Experiment Type
Animal & Cell Experiment
Phenotype Related
Chronic Kidney Disease; End-stage Renal Disease; Hypertensive Kidney Fibrosis; Chronic Kidney Diseases; Chronic Hypertension; Fibrosis; Ckds; Kidney Fibrosis
Paper Title Cn
Paper Title En
Kaempferol inhibits renal fibrosis by suppression of the sonic hedgehog signaling pathway
Bilingual Status
semi_complete