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Article Publish Status: FREE
Abstract Title:

Cyanidin-3-galactoside fromameliorates silica-induced pulmonary fibrosis by modulating the TGF-β/mTOR and NRF2/HO-1 pathways.

Abstract Source:

Food Sci Nutr. 2022 Aug ;10(8):2558-2567. Epub 2022 Mar 30. PMID: 35959254

Abstract Author(s):

Yanmin Cui, Jin Zhao, Jing Chen, Yanwen Kong, Mingyue Wang, Yan Ma, Xianjun Meng

Article Affiliation:

Yanmin Cui

Abstract:

Cyanidin-3-galactoside (C3G), the most abundant anthocyanin ina, has many beneficial health effects, such as antioxidation. C3G was extracted fromand applied (100, 200, and 400 mg/kg body weight) to 50-μl silica particles (SP) solution-exposed mice to research its antifibrotic properties using histological analysis, hydroxyproline assay, quantitative real-time polymerase chain reaction, and western blot analysis. The results showed that C3G treatment significantly ameliorated pulmonary fibrosis and cell infiltration into the lungs of mice. It also relieved SP-induced epithelial-mesenchymal transition (EMT), 400 mg/kg C3G treatment increasing epithelial-cadherin mRNA expression and decreasing α-smooth muscle actin mRNA expression to the level of that in the control group. Western blot analysis showed that exposure to SP increased the production of transforming growth factor-β1 (TGF-β1) and phosphorylated mammalian target of rapamycin (mTOR) by 4.71- and 4.15-fold, respectively, in the lungs of mice, which were significantly inhibited by C3G treatment. Moreover, 400 mg/kg C3G treatment up-regulated two important antioxidant mediators, nuclear factor erythroid-2-related factor 2 (NRF2; 4.91-fold) and heme oxygenase-1 (HO-1; 4.81-fold). The mechanism study indicated that C3G might inhibit the TGF-β/mTOR signaling via the NRF2/HO-1 pathway and that SP-induced pulmonary EMT was ameliorated by inhibiting the TGF-β/mTOR signaling pathway. Our findings could provide new avenues for C3G as a functional food for preventing or mediating the progression of SP-induced pulmonary fibrosis.

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