当前位置:主页 > 医学论文 > 西医药论文 >

α-2b干扰素对乙型肝炎模型鸭肝组织炎症和肝纤维化的治疗作用

发布时间:2018-08-14 18:10
【摘要】:目的:通过鸭乙型肝炎病毒(DHBV)阳性血清注射建立鸭乙型肝炎模型,探讨α-2b干扰素治疗DHBV所致鸭肝炎症及肝纤维化的作用,为干扰素的临床应用提供依据。方法:10日龄北京麻鸭40只随机分为对照组(6只)和感染组(34只),感染组使用DHBV阳性血清1周内3次注射的方法,制备鸭乙型肝炎模型。2周后,采用斑点杂交法检测DHBV-DNA水平确认感染鸭共32只,随机将感染动物分为模型对照组(10只)、低剂量及高剂量α-2b干扰素组(各11只),α-2b干扰素组鸭分别肌肉注射低剂量(1×105 U·100g-1)和高剂量(5×105 U·100g-1)α-2b干扰素治疗。30d治疗结束后,采用斑点杂交法检测各组鸭血清DHBV-DNA水平,检测天门冬氨酸氨基转移酶(AST)、谷氨酸氨基转移酶(ALT)和肝纤维化指标层黏蛋白(LN)及Ⅲ型前胶原肽(PCⅢ)水平,取肝组织检测白细胞介素6(IL-6)、白细胞介素12(IL~(-1)2)和肿瘤坏死因子α(TNF-α)水平,观察组织病理形态表现。结果:与造模前比较,造模后鸭血清DHBV-DNA水平明显升高,表明造模成功。α-2b干扰素治疗结束后,与模型组比较,低和高剂量α-2b干扰素组鸭血清DHBV-DNA水平明显下降(P0.05),血清中AST和ALT水平降低(P0.05),其中高剂量α-2b干扰素组LN及PCⅢ型水平明显降低(P0.05),肝组织中IL-6和TNF-α水平明显降低(P0.05),IL~(-1)2水平无明显变化(P0.05)。组织病理形态表现,与模型组比较,低和高剂量α-2b干扰素组鸭肝组织中纤维化明显减轻。结论:α-2b干扰素可以减轻DHBV所致的鸭肝组织炎症和肝纤维化,本研究为干扰素的进一步开发和临床应用提供了理论依据。
[Abstract]:Objective: to establish duck hepatitis B model by injecting duck hepatitis B virus (DHBV) positive serum to investigate the effect of 伪 -2b interferon on duck liver inflammation and hepatic fibrosis induced by DHBV, and to provide evidence for clinical application of interferon. Methods 40 10 day old Beijing duck were randomly divided into control group (6) and infected group (34). The infected group was injected with DHBV positive serum 3 times within one week to prepare duck hepatitis B model after .2 weeks. The DHBV-DNA level of 32 infected ducks was detected by dot blot hybridization. The infected animals were randomly divided into model control group (n = 10), low dose interferon group (n = 11) and high-dose interferon 伪 -2b group (n = 11 each). The ducks of 伪 -2b interferon group were injected intramuscularly with low dose (1 脳 10 5 U 100g-1) and high dose (5 脳 10 5 U 100g-1) 伪 -2b interferon for 30 days. The levels of serum DHBV-DNA, aspartate aminotransferase (AST), glutamate aminotransferase (ALT), laminin (LN) and procollagen 鈪,

本文编号:2183691

资料下载
论文发表

本文链接:https://www.wllwen.com/xiyixuelunwen/2183691.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户a325a***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com