目的 探讨糖尿病高糖高脂状态对四氯化碳(CCl4)诱导的化学性肝纤维化进展的影响.方法 采用高脂饲料及链脲佐菌素(STZ)建立糖尿病模型,四氯化碳诱导肝纤维化模型,高脂饲料、STZ及CCl4诱导糖尿病合并肝纤维化模型,动态监测各组大鼠体重、血糖及相关血清学指标;HE染色观察各组大鼠的肝脏病理学变化;Western blot、q-PCR检测各组大鼠肝组织中α-SMA和Collagen I的表达.结果与对照组大鼠相比,糖尿病组和糖尿病合并肝纤维化组大鼠体重明显下降,血糖血脂均升高,肝纤维化组无明显差异;HE染色及血清AST/ALT检测表明,与对照组大鼠肝组织相比,糖尿病大鼠、肝纤维化大鼠及糖尿病合并肝纤维化大鼠肝组织均有不同程度的肝损伤,以糖尿病合并肝纤维化组大鼠最为严重;3组大鼠肝组织α-SMA和Collagen I表达较对照组也不同程度增加,以糖尿病合并肝纤维化组大鼠最为明显,与单纯糖尿病组和肝纤维化组比较,差异有显著性.结论糖尿病可诱发肝损伤,加剧CCl4诱导的大鼠肝纤维化病变.%Aim To observe the effect of diabetes on carbon tetrachloride (CCl4)-induced rats chemical liv-er injury and liver fibrosis by establishing diabetes mer-ged with liver fibrosis rat model (double model). Methods High fat feeding combined with streptozoto-cin (STZ) was used to induce diabetes rat model,and liver fibrosis rat model was induced by CCl4. HE stai-ning was used to observe the rat liver pathological changes, and Western blot and q-PCR were used to detect liver fibrosis related factor genes α-SMA and Collagen Ⅰ expression. Results Compared with con-trol group, diabetes group, liver fibrosis group and double model group all had different levels of liver damage,especially double model group. Rat liver tis-sues of α-SMA and CollagenⅠexpression from differ-ent model groups also increased, especially those from double model group, and significant differences were detected compared to diabetes and liver fibrosis group. Conclusions Diabetes can cause liver damage and in-crease the occurrence and development of CCl4-in-duced rats liver fibrosis, and the mechanism may be related to the formation and/or degradation of extracel-lular matrix.
展开▼
