Hepatoprotective effect of infliximab, an anti-TNF-α agent, on carbon tetrachloride-induced hepatic fibrosis
Hepatoprotective effect of infliximab, an anti-TNF-α agent, on carbon tetrachloride-induced hepatic fibrosis
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DOI：
10.1007/s10753-008-9067-1
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发表时间：
2008-08-01
期刊：
影响因子：
5.1
通讯作者：
Isik, Ahmet
中科院分区：
文献类型：
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作者：
Bahcecioglu, Ibrahim Halil;Koca, Suleyman Serdar;Isik, Ahmet
目的：评价抗肿瘤坏死因子-α制剂英夫利昔单抗对四氯化碳(CCl(4))诱导的大鼠肝纤维化的影响。将大鼠随机分为3组(n=9)。对照组只接受腹膜腔注射。橄榄油。反复ip诱导大鼠肝纤维化。其余两组皮下注射CCl(4)1.5ml/kg(与橄榄油1：3混合)，共5周，皮下注射生理盐水或英夫利昔单抗2 mg/kg。英夫利昔单抗可降低天冬氨酸氨基转移酶和丙氨酸氨基转移酶水平(P<；0.05)。英夫利昔单抗治疗组大鼠肝组织坏死、炎症、纤维化评分及α-平滑肌肌动蛋白表达均低于CCI(4)治疗组(P<0.01，P<0.001，P<0.01，P<0.001)。然而，在肝组织和血浆丙二醛以及血清肿瘤坏死因子-α水平方面没有显著差异，而英夫利昔单抗相对降低了转化生长因子-β(1)的水平(373.0+/-153.1 pg/ml对280.8+/-127.1 pg/ml)。英夫利昔单抗治疗可减轻CCI(4)诱导的肝纤维化的坏死性炎症和纤维化形成，因此可能是一种有效的治疗抗纤维化药物。
To assess the effect of infliximab, an anti-tumor necrosis factor (TNF)-alpha agent, on the carbon tetrachloride (CCl(4))-induced hepatic fibrosis in rats. Rats were randomized into three groups (n=9). The control group received only intraperitoneal (i.p.) olive oil. Hepatic fibrosis was induced by repeated i.p. injections of 1.5 ml/kg CCl(4) (1:3 mixture with olive oil) for 5 weeks in the remaining two groups which were also injected subcutaneous saline or 2 mg/kg infliximab. Infliximab reduced the levels of aspartate aminotransferase and alanine aminotransferase (p < 0.05 for both). The scores of hepatic necrosis, inflammation and fibrosis, and expression of alpha-smooth muscle actin were lower in the infliximab-treated group than the CCI(4)-treated group (p < 0.01, p < 0.001, p < 0.01, p < 0.001, respectively). However, there was no significant difference in terms of liver tissue and plasma malondialdehyde, and serum TNF-alpha levels, while infliximab relatively reduced the level of transforming growth factor-beta(1) (373.0 +/- 153.1 vs. 280.8 +/- 127.1 pg/ml). Treatment with infliximab attenuated the necro-inflammation and fibrogenesis in the CCI(4)-induced hepatic fibrosis, and thus it might be effective as a therapeutic anti-fibrotic agent.