期刊
JOURNAL OF FUNCTIONAL FOODS
卷 83, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.jff.2021.104547
关键词
Urolithin A; Renal fibrosis; UUO model; HK-2 cells; TGF-beta
资金
- National Natural Science Foundation of China [31770381]
UA treatment significantly alleviates renal tissue damage induced by UUO, reducing macrophage infiltration and proinflammatory cytokine expression, inhibiting EMT progression, and regulating the TGF-beta 1/Smad and MAPK signaling pathways to suppress fibrosis.
Urolithin A (UA) is a bioavailable product of the metabolism of ellagitannins by the gut microbiota, and UA has anti-inflammatory and antioxidant activities. In this study, we investigated whether UA exerted an anti-renal fibrosis effect in a rat model of unilateral ureteral obstruction (UUO) and HK-2 cells treated with TGF-beta 1. In vivo, UA treatment significantly ameliorated UUO-induced renal tissue impairment and decreased macrophage infiltration and proinflammatory cytokine expression. UA attenuated epithelial-mesenchymal transition (EMT) progression by regulating the expression of E-cadherin and alpha-SMA. Moreover, UA treatment significantly decreased the levels of TGF-beta 1, p-Smad2/3, and p-P38/JNK/ERK but increased the level of Smad7. In vitro, UA treatment inhibited TGF-beta 1-induced HK-2 cell fibrosis and proliferation. Furthermore, UA treatment also led to a reduction in the expression of TGF-beta 1, p-Smad3, and p-P38/JNK/ERK, which was accompanied by an increase in the expression of Smad7. These results demonstrate that UA exerts protective effects on renal fibrosis by inhibiting the TGF-beta 1/Smad and MAPK signaling pathways.
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