糖皮质激素对慢加急性肝衰竭大鼠CD163和细胞因子的影响及意义
发布时间：2018-11-01 12:49
【摘要】：目的研究糖皮质激素（地塞米松）对慢加急性肝衰竭大鼠模型CD163分子及促炎与抗炎因子的影响及意义。 方法SPF级雄性Wistar大鼠30只，，分为三组，正常对照组与慢加急性肝衰竭（ACLF）模型组各6只，地塞米松治疗组18只。先用四氯化碳（CCL4）植物油溶液腹腔注射8周，再给予D-氨基半乳糖（D-GalN）和脂多糖（LPS）联合冲击，制备慢加急性肝衰竭模型。地塞米松治疗组按给药时间的不同分为三组：造模后0h治疗组，造模后4h治疗组，造模后8h治疗组。各组在造模后24h，处死大鼠，检测血清中ALT、AST、TBIL，大鼠肝组织H-E染色观察病理改变，实时定量PCR法检测肝组织中CD163分子表达水平，ELISA法检测血清TNF-a及IL-10水平。 结果大鼠慢加急性肝衰竭（ACLF）模型制备良好，在肝组织纤维化基础上出现了片状坏死，炎细胞浸润明显，肝功能指标显著升高，血清中TNF-a水平明显升高。造模后0h地塞米松治疗组肝脏组织学明显好转，生化指标和血清TNF-a水平较模型组明显下降，血清IL-10水平及肝组织CD163分子表达增加，与ACLF模型组相比，差异有统计学意义（P0.05）；造模后4h地塞米松治疗组与8h治疗组上述指标与ACLF模型组相比，差异无统计学意义。 结论慢加急性肝衰竭早期应用地塞米松可平衡促炎因子与抑炎因子的分泌，同时也促进肝组织CD163分子的表达，对肝脏有保护作用。
[Abstract]:Objective to study the effect and significance of glucocorticoid (dexamethasone) on CD163 molecules, proinflammatory and anti-inflammatory factors in chronic and acute hepatic failure rats. Methods Thirty SPF grade male Wistar rats were divided into three groups: normal control group (n = 6), chronic and acute hepatic failure (ACLF) model group (n = 6) and dexamethasone treatment group (n = 18). The model of chronic and acute hepatic failure was established by intraperitoneal injection of carbon tetrachloride (CCL4) with vegetable oil solution for 8 weeks and then combined shock of D-galactosamine (D-GalN) and lipopolysaccharide (LPS). The dexamethasone treatment group was divided into three groups according to the time of administration: the treatment group at 0 h after model making, the treatment group at 4 h after model making, and the treatment group at 8 h after model making. The rats in each group were killed 24 hours after the model. H-E staining in serum of ALT,AST,TBIL, rats was detected. The expression of CD163 molecule in liver tissue was detected by real-time quantitative PCR, and the levels of TNF-a and IL-10 in serum were detected by ELISA method. Results the (ACLF) model of chronic and acute hepatic failure in rats was well prepared, with flake necrosis on the basis of hepatic fibrosis, obvious infiltration of inflammatory cells, a significant increase in liver function, and a marked increase in the level of TNF-a in serum. The liver histology of dexamethasone treatment group was obviously improved, the biochemical index and serum TNF-a level were significantly lower than those of the model group, the serum IL-10 level and the expression of CD163 molecule in liver tissue were increased, compared with the ACLF model group. The difference was statistically significant (P0.05). There was no significant difference in the above indexes between the dexamethasone treatment group and the ACLF model group 4 hours after the establishment of the model. Conclusion early application of dexamethasone in chronic and acute liver failure can balance the secretion of pro-inflammatory factor and anti-inflammatory factor, promote the expression of CD163 molecule in liver tissue, and protect the liver.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R575.3
本文编号：2303975
[Abstract]:Objective to study the effect and significance of glucocorticoid (dexamethasone) on CD163 molecules, proinflammatory and anti-inflammatory factors in chronic and acute hepatic failure rats. Methods Thirty SPF grade male Wistar rats were divided into three groups: normal control group (n = 6), chronic and acute hepatic failure (ACLF) model group (n = 6) and dexamethasone treatment group (n = 18). The model of chronic and acute hepatic failure was established by intraperitoneal injection of carbon tetrachloride (CCL4) with vegetable oil solution for 8 weeks and then combined shock of D-galactosamine (D-GalN) and lipopolysaccharide (LPS). The dexamethasone treatment group was divided into three groups according to the time of administration: the treatment group at 0 h after model making, the treatment group at 4 h after model making, and the treatment group at 8 h after model making. The rats in each group were killed 24 hours after the model. H-E staining in serum of ALT,AST,TBIL, rats was detected. The expression of CD163 molecule in liver tissue was detected by real-time quantitative PCR, and the levels of TNF-a and IL-10 in serum were detected by ELISA method. Results the (ACLF) model of chronic and acute hepatic failure in rats was well prepared, with flake necrosis on the basis of hepatic fibrosis, obvious infiltration of inflammatory cells, a significant increase in liver function, and a marked increase in the level of TNF-a in serum. The liver histology of dexamethasone treatment group was obviously improved, the biochemical index and serum TNF-a level were significantly lower than those of the model group, the serum IL-10 level and the expression of CD163 molecule in liver tissue were increased, compared with the ACLF model group. The difference was statistically significant (P0.05). There was no significant difference in the above indexes between the dexamethasone treatment group and the ACLF model group 4 hours after the establishment of the model. Conclusion early application of dexamethasone in chronic and acute liver failure can balance the secretion of pro-inflammatory factor and anti-inflammatory factor, promote the expression of CD163 molecule in liver tissue, and protect the liver.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R575.3
【参考文献】
相关期刊论文 前1条
1 聂青和;;肝衰竭综合治疗进展[J];实用肝脏病杂志;2013年01期
本文编号：2303975
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