Chinese researchers investigated the anti-fibrotic effects of curcumin on epithelial-to-mesenchymal transition (EMT) induced by transforming growth factor-B1 (TGF-B1), as well as the mechanism by which it influences the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Their findings were published in the journal Biological and Pharmaceutical Bulletin.
According to animal studies, curcumin has protective effects against the development of renal fibrosis.
However, the mechanisms underlying these effects are unknown.
To address this, the researchers treated human kidney tubular epithelial cells (HKCs) with either TGF-B1 or curcumin alone and with a combination of both.
They used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to assess the effect of curcumin on cell proliferation.
They also used immunocytochemistry, real-time PCR and Western blot to analyze the expression of E-cadherin, cytokeratin, vimentin, alpha-smooth muscle actin (a-SMA), fibroblast-specific protein 1 (FSP1) and key proteins of the Akt/mammalian target of rapamycin (mTOR) pathway.
The researchers found that low-dose curcumin (3.125 and 25?micromol/L) effectively promoted HKC proliferation.
After 72 hours of incubating HKCs with TGF-B1 and curcumin, curcumin caused the cells to maintain epithelial morphology in a dose-dependent manner.
It also decreased the expression of vimentin, a-SMA and FSP1 and increased the expression of E-cadherin and cytokeratin.
The researchers also noted that curcumin reduced Akt, mTOR and P70S6K phosphorylation, effectively suppressing the Akt/mTOR pathway in HKCs.