糖皮質(zhì)激素對(duì)慢加急性肝衰竭大鼠CD163和細(xì)胞因子的影響及意義
發(fā)布時(shí)間：2018-11-01 12:49
【摘要】：目的研究糖皮質(zhì)激素（地塞米松）對(duì)慢加急性肝衰竭大鼠模型CD163分子及促炎與抗炎因子的影響及意義。 方法SPF級(jí)雄性Wistar大鼠30只，，分為三組，正常對(duì)照組與慢加急性肝衰竭（ACLF）模型組各6只，地塞米松治療組18只。先用四氯化碳（CCL4）植物油溶液腹腔注射8周，再給予D-氨基半乳糖（D-GalN）和脂多糖（LPS）聯(lián)合沖擊，制備慢加急性肝衰竭模型。地塞米松治療組按給藥時(shí)間的不同分為三組：造模后0h治療組，造模后4h治療組，造模后8h治療組。各組在造模后24h，處死大鼠，檢測(cè)血清中ALT、AST、TBIL，大鼠肝組織H-E染色觀察病理改變，實(shí)時(shí)定量PCR法檢測(cè)肝組織中CD163分子表達(dá)水平，ELISA法檢測(cè)血清TNF-a及IL-10水平。 結(jié)果大鼠慢加急性肝衰竭（ACLF）模型制備良好，在肝組織纖維化基礎(chǔ)上出現(xiàn)了片狀壞死，炎細(xì)胞浸潤(rùn)明顯，肝功能指標(biāo)顯著升高，血清中TNF-a水平明顯升高。造模后0h地塞米松治療組肝臟組織學(xué)明顯好轉(zhuǎn)，生化指標(biāo)和血清TNF-a水平較模型組明顯下降，血清IL-10水平及肝組織CD163分子表達(dá)增加，與ACLF模型組相比，差異有統(tǒng)計(jì)學(xué)意義（P0.05）；造模后4h地塞米松治療組與8h治療組上述指標(biāo)與ACLF模型組相比，差異無(wú)統(tǒng)計(jì)學(xué)意義。 結(jié)論慢加急性肝衰竭早期應(yīng)用地塞米松可平衡促炎因子與抑炎因子的分泌，同時(shí)也促進(jìn)肝組織CD163分子的表達(dá)，對(duì)肝臟有保護(hù)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.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R575.3
本文編號(hào)：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.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R575.3
【參考文獻(xiàn)】
相關(guān)期刊論文 前1條
1 聶青和;;肝衰竭綜合治療進(jìn)展[J];實(shí)用肝臟病雜志;2013年01期
本文編號(hào)：2303975
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