Study On The Mechanism Of Ligustrazine On Human Embryonic Lung Fibroblast MRC-5

Objective:Through investigating Ligustrazine injection on MRC-5embryonic lung fibroblasts intervention effect,we eager for understanding Ligustrazine anti fibrosis mechanism,in order to provide effective treatment for interstitial pneumonia,so as to reduce the case fatality rate and help alleviate patients pain and economic burden,which provides new thinking for clinical treatment.Methods:MRC-5 embryonic lung fibroblasts as the research object the experiment of ligustrazine injection as experimental drug,low molecular heparin as control drug,respectively,set up A blank group,the low molecular heparin group M and ligustrazine injection group C.On the basis of cell recovery and passage,using low molecular heparin and ligustrazine injection intervente embryonic lung fibroblasts for 24 h,CCK-8 method detecting cell proliferation;Annexin V APC / 7-AAD method detecting cell apoptosis,Sirius red staining to detect collagen secretion;SOD the kits level of SOD,MDA kits MDA;ELISA method to detect CTGF,NF-κB、TGF-β1 level;QPCR detection CTGF mRNA,NF-κB mRNA,TGF-β1 mRNA level.Results: ligustrazine injection can inhibit the embryonic lung fibroblasts proliferation and promote apoptosis of the fibroblast,reducethe secretion of extracellular matrix,improve the level of cell oxidation,inhibition of CTGF,NF-κB,TGF-β1 and its mRNA.In contrast,low molecular heparin can inhibit cell proliferation,but its promoting apoptosis ratio is low,causing cell death number,cell significantly lower SOD level,can inhibit the CTGF,NF-κB,TGF-β1 and its mRNA,CTGF and TGF-β1 inhibition compared with ligustrazine is poor,NF-κB no obvious difference was found between ligustrazine restraining effect.Conclusion: ligustrazine injection has obvious inhibitory effect on fibroblasts,in promoting apoptosis,reducing collagen secretion function significantly and suppressing a variety of cytokines and their mRNA.ligustrazine injection has a clear role in resistance to pulmonary fibrosis.Low molecular heparin as experiment contrast and drugs,although also can inhibit human lung fibroblasts proliferation,inhibiting some the secretion of cytokines,but it can increase cell oxidative damage and has obvious cytotoxicity,so not as a recommended drug resistance of pulmonary fibrosis.