丙泊酚对Wistar大鼠肝癌模型中Bax与Bcl-2表达的影响

摘要

Objective:To investigate the influence of propofol with different concentrations on the expression of Bcl-2 and Bax in Wistar rat model of hepatic carcinoma. Method:50 Wistar rats were divided into 5 groups according to random number table method,each group had 10 rats,the normal group(the group A),the liver cancer model group(the group B), the low dose Propofol group:3 mg/kg(the group C1),the moderate dose Propofol group:6 mg/kg(the group C2),the high dose Propofol group:12 mg/kg(the group C3). The liver tissue were collected in 24 h after the last injection and observed by morphology and hematoxylin and eosin(HE)staining. S-P immunohistochemistry was used to examine the expression of Bcl-2 and Bax in liver tissue of different groups of Wistar rats. Result:(1)Morphology and HE staining:compared with the group A,the group became B ragged and yellow spots appeared on some surfaces. Liver cells appeared steatosis,spotty necrosis and inflammatory cell infiltration by HE staining. Compared with the group B,there were less steatosis and spotty necrosis in the group C(C1,C2,C3).(2)TUNEL staining showed that increased the dosage of Propofol,apoptosis cells of liver cancer cells increased,the AI was increased gradually,the difference was statistical significance(P<0.05).(3) Compared with the group A,the expression of Bcl-2 increased,and the expression of Bax decreased in the group B,the difference was statistically significant(P<0.05). Compared with the group B,the Bcl-2 expression decreased liver cells in the group C(C1,C2 and C3),and increased with the increase of dosage of Propofol showed a trend of decline,the difference was statistically significant(P<0.05);Bax expression was raised,and increased with the increase of Propofol dose increased trend,the difference was statistically significant(P<0.05). Conclusion:The rate of Bcl-2/Bax is decreased by Propofol, which could inhibit the proliferation of HCC cells.%目的：探讨不同浓度丙泊酚对Wistar大鼠肝癌模型中凋亡促进基因Bax和凋亡抑制基因Bcl-2表达的影响。方法：将50只雄性Wistar大鼠按随机数字表法分为五组，每组10只，分别为正常对照组（A组），肝癌模型组（B组），低剂量丙泊酚（3 mg/kg）组（C1组），中等剂量丙泊酚（6 mg/kg）组（C2组），高剂量丙泊酚（12 mg/kg）组（C3组）。给药结束后24 h处死大鼠，取肝脏标本观察肝脏特征，并做组织切片行苏木精-伊红（HE）染色及S-P免疫组化检测Bcl-2及Bax的表达，TUNEL法检测肝细胞凋亡指数（AI）。结果：（1）大体标本检查及H E染色：与A组比较，B组大鼠肝脏表面粗糙，部分肝叶表面出现黄色斑点，肝细胞脂肪变性，点状坏死及炎细胞浸润，少量胶原纤维增生；与B组比较，C1、C2、C3组肝细胞变性坏死以及胶原纤维增生程度有所减轻；（2）TUNEL检测结果：随丙泊酚剂量增加，肝癌细胞中凋亡细胞逐渐增多，AI逐渐递增，具有显著差异性（P<0.05）；（3）与A组比较，B组肝脏细胞Bcl-2表达上调，Bax表达下降，差异均有统计学意义（P<0.05）；与B组比较，C组（C1、C2、C3）肝脏细胞Bcl-2表达均下降，且随着丙泊酚剂量的增加而呈递减趋势，差异有统计学意义（P<0.05）；Bax表达均上调，且随着丙泊酚剂量的增加而呈递增趋势，差异有统计学意义（P<0.05）。结论：丙泊酚可导致Wistar大鼠肝癌细胞中Bcl-2/Bax表达比例降低，促进肝癌细胞的凋亡，进而抑制肝癌细胞的增殖能力。