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目的:证明四氯化碳(carbon tetrachloride,CCl4)诱导的肝纤维化小鼠对致死性D-氨基半乳糖/脂多糖(D-galactosamine and lipopolysaccharide,D-GalN/LPS)攻击的耐受性.方法:建立CCl4诱导的肝纤维化小鼠模型,于纤维化6 wk时以致死剂量的D-GalN(700 mg/kg)/LPS(50μg/kg)进行攻击,以同样处理的正常小鼠作为对照,即实验共分为4组:正常对照组(Nor)、急性损伤组(Nor+D-GalN/LPS)、肝纤维化组(Fib)、肝纤维化+急性攻击组(Fib+D-GalN/LPS).根据攻击前后小鼠生存率、转氨酶水平及肝组织学的变化来评估正常和纤维化小鼠对致死性D-GalN/LPS损伤的耐受性.结果:生存分析显示,Fib+D-GalN/LPS组的生存率显著高于Nor+D-GalN/LPS组(100%vs20%).血清转氨酶结果表明,Fib+D-GalN/LPS组肝损伤程度明显轻于Nor+D-GalN/LPS组,其sALT水平分别为(6630 U/L±1675 U/L)和(22429 U/L±5446 U/L)(P<0.01).接受攻击的纤维化和正常小鼠的sALT分别升高了14.3倍和455.9倍.肝组织学检查结果也证明,接受致死性D-GalN/LPS攻击的纤维化小鼠的肝损伤较同样处理的正常小鼠明显减轻.结论:CCl4诱导的肝纤维化可保护小鼠抵抗致死性D-GalN/LPS损伤的攻击.
OBJECTIVE: To demonstrate the tolerability of lethal D-galactosamine and lipopolysaccharide (D-GalN / LPS) challenge in liver fibrosis mice induced by carbon tetrachloride (CCl4). Methods: The CCl4-induced hepatic fibrosis mouse model was established and challenged with lethal dose of D-GalN (700 mg / kg) / LPS (50 μg / kg) at 6 weeks after fibrosis. The control group consisted of four groups: Nor, D-GalN / LPS group, Fib group, Fibronectin + D- GalN / LPS) .We evaluated the tolerability of lethal D-GalN / LPS in normal and fibrotic mice according to the survival rate, aminotransferase level and liver histology before and after challenge.Results: Survival analysis showed that Fib LPS group was significantly higher than that of Nor + D-GalN / LPS group (100% vs20%). The results of serum transaminase showed that the degree of hepatic injury in Fib + D-GalN / -GalN / LPS group, the sALT levels were 6630 U / L ± 1675 U / L and 22429 U / L ± 5446 U / L, respectively (P <0.01) sALT increased 14.3 times and 455.9 times respectively The results of liver histology also demonstrated that liver damage in fibrosis mice challenged with lethal D-GalN / LPS was significantly reduced compared with normal mice treated with the same treatment.Conclusion: CCl4-induced hepatic fibrosis can protect mice from lethality Sex D-GalN / LPS Damage Attack.