Study on the in vitro mechanism of Physochlaina infundibularis Kuang in intervening pulmonary fibrosis
[Objective]To study the effects of Physochlaina infundibularis Kuang on Recombinant Mouse TGF-β1(TGF-β1)as well as cigarette smoke extract(CSE)on mouse embryonic fibroblasts(NIH-3T3)and human bronchial epithelial cells(BEAS-2B)and related mechanisms.[Methods]MTT method was used to screen the safe concentrations of Physochlaina infundibularis Kuang alkaloids,non-alkaloids,and total extracts on NIH-3T3 cells;NIH-3T3 cells were induced by TGF-[31 for 24 h,stained with Sirius Scarlet,and the relative collagen deposition rate was calculated;MTT method was used to screen the safe concentrations of 7 Physochlaina infundibularis Kuang alkaloidal monomers on BEAS-2B cells,respectively;BEAS-2B cells were treated with CSE After 24,[3-galactosidase staining was performed;Western blot method was used to detect the expression levels of TGF-β1,Smad3 and NLRP3 proteins.[Results]Physochlaina infundibularis Kuang alkaloids,non-alkaloids,and total extracts significantly inhibited TGF-[31-induced collagen deposition in NIH-3T3 cells(all P＜0.05);scopolamine and dehydro-atropine significantly inhibited CSE-induced senescence in BEAS-2B cells(all P＜0.05),and were able to significantly inhibit the expression of TGF-β1,Smad3,and NLRP3 proteins(all P＜0.05).[Conclusion]Physochlaina infundibularis Kuang may regulate the progression of pulmonary fibrosis in vitro by inhibiting the TGF-β1/Smad3 pathway.
国家科技期刊平台
NSTL
万方数据
