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Abstract Title:

Kaempferol Modulates Autophagy and Alleviates Silica-Induced Pulmonary Fibrosis.

Abstract Source:

DNA Cell Biol. 2019 Sep 27. Epub 2019 Sep 27. PMID: 31560574

Abstract Author(s):

Hangqi Liu, He Yu, Zhenju Cao, Junxu Gu, Lin Pei, Mei Jia, Ming Su

Article Affiliation:

Hangqi Liu

Abstract:

Silicosis is an occupational disease characterized as inflammatory cells infiltration and severe progressive pulmonary fibrosis. Kaempferol (Kae), a flavonoid exists in many plants and fruits, has been proved to have anti-inflammatory and antifibrosis functions. However, the effects of Kae on silicosis remain unclear. In the present study, we analyzed the therapeutic effects of Kae in 1-, 7-, and 28-day silicosis models, respectively. In the 1-day model, Kae treatment did not vary the wet-to-dry weight ratios of the lung, apoptotic rate, autophagy, or the expression of inflammatory factors. In contrast, Kae significantly inhibited pulmonary inflammation in the 7-day silicosis models and inhibited silica-induced pulmonary fibrosis in the 28-day models. Besides, we found that Kae partially restored silica-induced LC3 lipidation without increasing the p62 levels. Blocking autophagy with chloroquine antagonized the inhibitory effects of Kae on inflammation, suggesting that autophagy might be required in the therapeutic effects of Kae on silicosis. These findings indicated that Kae inhibits the progression of silica-induced pulmonary fibrosis, which may provide experimental evidences for Kae in the treatment of silicosis.

Study Type : Animal Study
Additional Links
Pharmacological Actions : Anti-Fibrotic : CK(46) : AC(29)

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