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目的:研究氧化苦参碱对HBV转基因鼠表达HBsAg, HBeAg,HBcAg的抑制作用,探讨氧化苦参碱抗HBV的机制. 方法:用显微注射法建立HBV转基因鼠动物模型,并进行HBV整合和表达鉴定.获得的HBV复制型转基因鼠随机分成3组,分别用生理盐水(9只),氧化苦参碱50 mg/kg (8只)和100 mg/kg(9只)腹腔注射,1次/d,30 d后处死,取肝组织定量测定HBsAg和HBeAg的量,免疫组织化学观察肝组织表达HBsAg和HBcAg. 结果:HBV转基因鼠经氧化苦参碱治疗后,与生理盐水组相比,肝脏组织HBsAg的量有所降低,但统计学无显著差异(F=1.29,P>0.05);而HBV转基因鼠经氧化苦参碱高和低剂量组治疗后,肝脏组织HBeAg量明显降低(F=9.09, P<0.01),但在氧化苦参碱高和低剂量组之间无显著性差异(F=1.58,P>0.05).肝脏组织免疫组化HBsAg和HBcAg 检测结果显示生理盐水组,氧化苦参碱低和高剂量组肝组织内HBsAg阳性细胞数变化不明显,统计学无显著性差异(X2=1.61,P>0.05).氧化苦参碱高剂量组肝组织内HBcAg 阳性细胞数明显低于生理盐水组(X2=4.73,P<0.05),而生理盐水组与氧化苦参碱低剂量组,氧化苦参碱低和高剂量组之间均无显著性差异. 结论:氧化苦参碱对HBV转基因鼠HBV的表达有抑制作用
Objective: To study the inhibitory effect of oxymatrine on the expression of HBsAg, HBeAg and HBcAg in HBV transgenic mice and to explore the mechanism of oxymatrine anti-HBV. Methods: To establish an animal model of HBV transgenic mice by microinjection and to perform HBV integration and Expression identification. The HBV replication-transgenic mice obtained were randomly divided into 3 groups: normal saline (9 mice), oxymatrine 50 mg/kg (8 rats) and 100 mg/kg (9 rats) intraperitoneally, once. After 30 days, the liver was sacrificed and the amount of HBsAg and HBeAg was measured quantitatively. The expression of HBsAg and HBcAg in the liver was observed by immunohistochemistry. Results: Compared to the saline group, the HBV transgenic mice were treated with oxymatrine. The amount of HBsAg in liver tissue decreased, but there was no statistically significant difference (F=1.29, P>0.05). However, after treatment with high and low doses of oxymatrine in HBV transgenic mice, the amount of HBeAg in liver tissue was significantly reduced (F =9.09, P<0.01), but there was no significant difference between high and low doses of oxymatrine (F=1.58, P>0.05). Liver tissue immunohistochemistry results of HBsAg and HBcAg showed saline group, The number of HBsAg-positive cells in the liver tissue of low- and high-dose oxymatrine groups did not change significantly, and there was no significant difference in statistics. (X2=1.61, P>0.05). The number of HBcAg-positive cells in the liver tissue of the high-dose oxymatrine group was significantly lower than that of the normal saline group (X2=4.73, P<0.05), while the normal saline group and oxymatrine were low. There was no significant difference between the low-dose group and high-dose group of oxymatrine dose group. Conclusion: Oxymatrine inhibits the expression of HBV in HBV transgenic mice.