CAJ | 학술논문

目的：研究 p38MAPK对乙醛刺激的大鼠肝星状细胞（HSC）活性及 c-myc蛋白表达的影响，探讨影响酒精性肝纤维化的相关机制。方法用不同浓度的p38特异性阻断剂SB203580干预乙醛刺激的大鼠HSC，显微镜下观察细胞形态变化，MTT法测定细胞增殖，流式细胞术检测细胞周期分布，SABC法检测 c-myc蛋白表达。结果（1）乙醛刺激后的 HSC体积增大，增殖迅速，但随着加入 SB203580的药物浓度增大，细胞增殖变缓，体积变小，变形的细胞增多。（2）p38阻断剂 SB203580可抑制乙醛刺激的 HSC增殖，且高药物浓度组抑制效果更明显。（3）随着阻断剂浓度增高，G0及 G1期细胞增加，S期细胞逐渐减少，同时 c-myc蛋白表达阳性率减少。结论阻断 p38MAPK通路活性能抑制乙醛刺激的大鼠 HSC增殖，可能与下调 c-myc蛋白表达，阻止细胞由 G0/G1期进入 S期的DNA合成有关。
목적：연구 p38MAPK대을철자격적대서간성상세포（HSC）활성급 c-myc단백표체적영향，탐토영향주정성간섬유화적상관궤제。방법용불동농도적p38특이성조단제SB203580간예을철자격적대서HSC，현미경하관찰세포형태변화，MTT법측정세포증식，류식세포술검측세포주기분포，SABC법검측 c-myc단백표체。결과（1）을철자격후적 HSC체적증대，증식신속，단수착가입 SB203580적약물농도증대，세포증식변완，체적변소，변형적세포증다。（2）p38조단제 SB203580가억제을철자격적 HSC증식，차고약물농도조억제효과경명현。（3）수착조단제농도증고，G0급 G1기세포증가，S기세포축점감소，동시 c-myc단백표체양성솔감소。결론조단 p38MAPK통로활성능억제을철자격적대서 HSC증식，가능여하조 c-myc단백표체，조지세포유 G0/G1기진입 S기적DNA합성유관。
Objective To study the effect of p38MAPK on the activity and c-myc protein expression in rat acetaldehyde-induced hepatic stellate cell(HSC),and to investigate the alcoholic liver fibrosis related mechanism.Methods The different concentrations of SB203580 as the p38 specific blocker was adopted to conduct the intervention on rat acetaldehyde-induced HSC.The cellular mor-phological change was observed by the microscope.The cell proliferation was detected by MTT,the cell cycle was analyzed by flow cytometry(FCM),and the expression of c-myc protein was examined by the SABC method.Results (1)after acetaldehyde stimula-tion,HSC was increased in size and proliferated rapidly,but with the added SB203580 concentration increase,the cellular prolifera-tion was slowed down,the cells size was diminished and the deformed cells were increased.(2)The proliferation of acetaldehyde-in-duced HSC was inhibited by different doses of SB203580,and the higher concentration has the more significant inhibiting effect.(3) With the SB203580 concentration increase,the cells at the phase G0 and G1 were increased,while the cells at the phase S were de-creased,at the same time the expression positive rate of c-myc protein was decreased.Conclusion Blocking p38MAPK pathway ac-tivity could inhibit the proliferation of acetaldehyde-induced HSC,which may be related to the down-regulation of C-myc protein ex-pression and blocking the DNA synthesis in cells entering from G0/G1 phase to S phase.