Allicin Role In The Regulation Of Rat Hepatic Stellate Cell Collagen Generation

Background: The treatment of liver disease has been troubled by the problems of the medical profession inrecent years, have important research value for the formation of chronic liver disease, cirrhosis liverfibrosis, recognized by the medical profession, its mechanism has also been a certain consensus. Liverfibrosis, is widely recognized as the extracellular matrix of the liver cells decreased degradation caused bythe excessive precipitation. Liver fibrosis research focused on the synthesis and decomposition of collagenfibers, as well as factors that affect collagen synthesis and degradation, in order to find the way of earlydiagnosis and treatment of liver fibrosis. Cytokine mediated between cells, caused by the interactionbetween the cells and the matrix hepatic stellate cell activation liver fibrosis is the most critical part of thestudy, the event of repeated liver injury, may also result in HSC further activation of HSC. According to theclinical and experimental data, lipid peroxidation products can more easily activated HSC, which damageliver cells. Therefore, the use of antioxidants in the treatment process, to relieve the symptoms of liverinjury and liver fibrosis. Antioxidants, allicin is a very effective to obtain a wide range of applications withhigh antioxidant capacity in the clinical and experimental.Abstract: Observed diallyl trisulfide proliferation of rat hepatic stellate cells （HSC-T6）, apoptosis, toexplore diallyl trisulfide anti-liver fibrosis and its mechanism.Methods: HSC-T6, a rat hepatic stellate cell lines grown in the volume fraction of10%fetal calf serum and1×10⁵IU/L penicillin,100mg/L of streptomycin in DMEM in37℃,5%CO₂saturatedcultured understeam conditions. Divided into HSC-T6cells blank control group, the reagent control group, diallyltrisulfide drug experimental group. Diallyl trisulfide drug concentration of the experimental group were12,24μg/ml DATS. Without drug and add an equal volume of10%fetal calf serum and1×10⁵IU/L ofpenicillin,100mg/L, streptomycin in DMEM medium is the reagent control group. The reagent controlgroups joined1.35μl/ml dimethyl sulfoxide. By determined by MTT method to detect diallyl trisulfide onrat hepatic stellate cell proliferation; BrdU incorporation experimental tests was used to detect diallyltrisulfide treated rat hepatic stellate cell proliferation inhibition; Through Hoechst33342staining and flowcytometry detection Annexin V-FITC/PI double dye detection of diallyl trisulfide treated rat hepatic stellate cell apoptosis; transmission electron microscopywas used to observe diallyl trisulfide treated rathepatic stellate cells; Western blot experiments identify the Bcl-2、MAO、TIMP-1protein of rat hepaticstellate cells after treated by diallyl trisulfide..Results: HSC-T6DATS treated group compared with the control group and the solvent control group, theproliferation inhibition rate and apoptosis rate was significantly higher, there is a significant difference （P<0.01）; DATS concentration, HSC-T6rate of inhibition, apoptosis rate gradually increased; proliferationinhibition rate and apoptosis rate of the experimental group were exposed to DATS, high concentrations（concentration content24μg/ml DATS） was significantly higher than the control group, the reagent controlgroup and a low concentration of the experimental group; to MTT assay the role of different concentrationsof diallyl trisulfide24-hour rat hepatic stellate cells. Diallyl trisulfide can inhibit the rat hepatic stellatecells of the Bcl-2MAO TIMP-1protein productionConclusion: Diallyl trisulfide can inhibit the proliferation of HSC-T6cells, induction of apoptosis, and therole of a dose-dependent. Diallyl trisulfide inhibits the proliferation of HSC-T6mechanism may HSC-T6cell cycle arrest. Diallyl trisulfide inhibit the apoptosis related proteins and protein involved in collagenformation。...