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目的建立小鼠慢性、慢加急性肝衰竭模型。方法 36只BALB/C小鼠随机分为4组。实验8周组、12周组、急性攻击组(每组8只)给予腹腔注射20%四氯化碳(CCl4)油溶液,连续注射8周、12周、12周。12周时,急性攻击组再腹腔联合注射D-氨基半乳糖(D-Gal)和脂多糖(LPS);对照组(12只)注射橄榄油12周。给药结束后,取小鼠血液和肝脏,生化法检测血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和白蛋白(ALB)水平,光镜、电镜下观察肝组织病理改变。结果①3个实验组ALT[(1354.80±491.57)U/L、(706.45±160.33)U/L、(664.47±173.33)U/L]、AST[(698.88±86.54)U/L、(531.60±91.89)U/L、(862.78±146.31)U/L]均显著高于对照组[(82.55±5.25)U/L、(379.16±72.17)U/L],P﹤0.05;②8周时,3个实验组小鼠的肝脏增大、变硬、粘连,镜下肝细胞变性、坏死、凋亡,并有少量纤维组织增生;12周时肝脏变小、质硬、呈小颗粒或小结节状,镜下同时存在坏死、凋亡及再生肝细胞,再生肝细胞排列紊乱,大量纤维组织增生,并形成假小叶。在此基础上联合急性攻击后,可出现肝组织点状、小片状坏死。结论 CCl4能诱导小鼠形成慢性肝纤维化、肝硬化,并有较明显的阶段性变化,联合给予D-Gal和LPS可诱导慢加急性肝衰竭。
Objective To establish a chronic, slow and acute liver failure model in mice. Methods 36 BALB / C mice were randomly divided into 4 groups. The rats in experimental group were given intraperitoneal injection of 20% carbon tetrachloride (CCl4) oil solution for 8 weeks, 12 weeks and 12 weeks after 8 weeks, 12 weeks and 8 days. At 12 weeks, the rats in the acute attack group were injected intraperitoneally with D-galactose (D-Gal) and lipopolysaccharide (LPS). The control group (12 mice) were injected with olive oil for 12 weeks. After administration, the blood and liver of mice were taken out and the levels of serum ALT, AST and ALB were measured by biochemistry method. The results of light microscope and electron microscope Liver tissue pathology. Results ① The levels of ALT in the three experimental groups were (1354.80 ± 491.57) U / L, (706.45 ± 160.33) U / L, (664.47 ± 173.33) U / L] and AST [(698.88 ± 86.54) U / L, (531.60 ± 91.89 ) (U / L, (862.78 ± 146.31) U / L] were significantly higher than those in the control group [(82.55 ± 5.25) U / L, (379.16 ± 72.17) U / L], P < In the experimental group, the liver of the mice in the experimental group was enlarged, hardened and adhered, and the liver cells were denatured, necrotic and apoptotic, with a small amount of fibrous tissue hyperplasia. At 12 weeks, the liver became smaller and harder with small particles or nodules There were necrotic, apoptotic and regenerative hepatocytes in the microscope. The regenerated hepatocytes were disordered and a large number of fibrous tissues were hyperplasia and pseudolobules were formed. On this basis, combined with acute attack, there may be punctate liver, small pieces of necrosis. Conclusion CCl4 can induce chronic hepatic fibrosis and cirrhosis in mice, and there are more obvious stage changes. Combined administration of D-Gal and LPS can induce slow and acute hepatic failure.