Treating diabetes mellitus (DM) with Chinese medicine (CM) has had a few thousands years of history. Past Chinese medical texts had already recorded numerous medicinal herbs as well as recipes for treating DM and accumulated much clinical experience. In the following article, the prevention of DM using CM in the past 5 years is retrospectively studied, and mainly focuses on the usage of simple Chinese herbal extracts or monomers in terms of cellular as well as molecular biology.
OBJECTIVE: To explore the function of Tangnai- kang (TNK) in the prevention and treatment of re- nal interstitial fibrosis through transdifferentiation of the human renal tubular epithelial cell line HK-2 induced bytransforming growth factor-β1 (TGF-β1). METHODS: HK-2 cells cultured in dulbecco's modi- fied eagle medium/F12 (1:1) with 10% fetal calf se- rum were divided into six groups: blank control group, TGF-β1 group (TGF-β1 10 ng/mL), serum con- trol group (TGF-β1 10 ng/mL + 10% serum), treat- ment group 1 (TGF-β1 10 ng/mL + 5% TNK serum), treatment group 2 (TGF-β1 10 ng/mL+10% TNK se-rum), and treatment group 3 (TGF-β1 10 ng/mL+ 20% TNK serum). Cell proliferation was detected by 4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliu m bromide assay. Expression of a-smooth muscle ac- tin (a-SMA) and E-cadherin were observed by im- munohistochemical assay. The contents of collagen Ⅰ (Col Ⅰ), collagen Ⅲ(ColⅢ), and fibronectin (FN) in the culture medium supernatant were detected by ELISA. RESULTS: E-cadherin was expressed and α-SMA was not expressed in normal HK-2 cells. In HK-2 cells cultured with TGF-β1, α-SMA expression signifi- cantly increased, HK-2 cells significantly proliferat- ed, and secretion of Col Ⅰ, Col Ⅲ, and FN significantly increased compared with the blank control group (all P〈0.05). In the HK-2 cells cultured with TGF-β1 and TNK serum, the expression of α-SMA signifi- cantly decreased, the expression of E-cadherin sig- nificantly increased, and the cell proliferation and the secretion of Col Ⅰ, Col Ⅲ and FN were significant- ly inhibited compared with the TGF-β1 group (all P〈 0.05. CONCLUSION: TNK can inhibit cell proliferation and reduce secretion of Col Ⅰ, Col Ⅲ, and FN.This in- dicates that TNK can inhibit transdifferentiation of human renal tubular epithelial cells induced by TGF-β1, with the effect of preventing and treating renal interstitial fibrosis.
Lixia YangXinhuan MaTao ChengTonghua LiuLili WuWen SunMargetts Peter Joseph