中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2011年
3期
203-206
,共4页
胰腺炎,急性坏死性%肿瘤坏死因子α%细胞间黏附分子%大鼠%沙利度胺
胰腺炎,急性壞死性%腫瘤壞死因子α%細胞間黏附分子%大鼠%沙利度胺
이선염,급성배사성%종류배사인자α%세포간점부분자%대서%사리도알
Pancreatitis,acute necrotizing%Tumor necrosis factor-alpha%Intercellular adhesion molecules%Rat%Thalidomide
目的 探讨沙利度胺对大鼠急性坏死性胰腺炎(ANP)的保护作用及机制.方法 54只SD大鼠按数字表法随机分成ANP组、沙利度胺组和对照组,每组18只.采用5%牛磺胆酸钠胰胆管逆行注射方法建立ANP模型.沙利度胺组于建模后1 h予沙利度胺200 mS/kg体重灌胃.术后3、6、12 h分批处死大鼠,观察腹水量;ELISA法检测血清TNF-α、IL-6、IL-18水平;流式细胞术检测外周血CD4+、CD8+T细胞比例;RT-PCR法检测胰腺组织TNF-α mRNA表达;免疫组化法检测胰腺组织细胞间黏附分子1(ICAM-1)蛋白表达;行胰腺常规病理检查.结果 术后6 h,对照组的腹水量,血清TNF-α、IL-6、IL-18水平和CD4+、CD8+T 细胞比例,胰腺组织TNF-α mRNA及CAM-1蛋白表达,病理评分分别为(1.03±0.31)ml、(57.17±11.29)pg/ml、(24.45 ±4.14)pg/ml、(64.23 ±21.85)pg/ml、(47.58±9.21)%、(40.88±2.96)%、0.07±0.02、0.57±0.30、0.67±0.81;ANP组分别为(3.63±0.38)ml、(107.54±33.05)pg/ml、(47.30±11.40)pg/ml、(367.76±108.43)pg/ml、(54.90±7.15)%、(17.17±3.12)%、0.65±0.26、3.20±0.57、11.50±1.87;沙利度胺组分别为(1.45±0.53)ml、(80.60±20.48)pg/ml、(26.61±10.85)pg/ml、(321.82±85.20)pg/ml、(29.80±2.19)%、(15.52±1.96)%、0.35±0.23、2.37±0.67、8.00±3.03.ANP组除CD8+T细胞比例显著降低外,其余指标均较对照组显著增加(P值均<0.05).沙利度胺组指标均显著低于ANP组(P值均<0.05).结论 沙利度胺能通过抑制TNF-α表达,减少炎症递质的释放,从而减轻ANP大鼠的胰腺病理损害.
目的 探討沙利度胺對大鼠急性壞死性胰腺炎(ANP)的保護作用及機製.方法 54隻SD大鼠按數字錶法隨機分成ANP組、沙利度胺組和對照組,每組18隻.採用5%牛磺膽痠鈉胰膽管逆行註射方法建立ANP模型.沙利度胺組于建模後1 h予沙利度胺200 mS/kg體重灌胃.術後3、6、12 h分批處死大鼠,觀察腹水量;ELISA法檢測血清TNF-α、IL-6、IL-18水平;流式細胞術檢測外週血CD4+、CD8+T細胞比例;RT-PCR法檢測胰腺組織TNF-α mRNA錶達;免疫組化法檢測胰腺組織細胞間黏附分子1(ICAM-1)蛋白錶達;行胰腺常規病理檢查.結果 術後6 h,對照組的腹水量,血清TNF-α、IL-6、IL-18水平和CD4+、CD8+T 細胞比例,胰腺組織TNF-α mRNA及CAM-1蛋白錶達,病理評分分彆為(1.03±0.31)ml、(57.17±11.29)pg/ml、(24.45 ±4.14)pg/ml、(64.23 ±21.85)pg/ml、(47.58±9.21)%、(40.88±2.96)%、0.07±0.02、0.57±0.30、0.67±0.81;ANP組分彆為(3.63±0.38)ml、(107.54±33.05)pg/ml、(47.30±11.40)pg/ml、(367.76±108.43)pg/ml、(54.90±7.15)%、(17.17±3.12)%、0.65±0.26、3.20±0.57、11.50±1.87;沙利度胺組分彆為(1.45±0.53)ml、(80.60±20.48)pg/ml、(26.61±10.85)pg/ml、(321.82±85.20)pg/ml、(29.80±2.19)%、(15.52±1.96)%、0.35±0.23、2.37±0.67、8.00±3.03.ANP組除CD8+T細胞比例顯著降低外,其餘指標均較對照組顯著增加(P值均<0.05).沙利度胺組指標均顯著低于ANP組(P值均<0.05).結論 沙利度胺能通過抑製TNF-α錶達,減少炎癥遞質的釋放,從而減輕ANP大鼠的胰腺病理損害.
목적 탐토사리도알대대서급성배사성이선염(ANP)적보호작용급궤제.방법 54지SD대서안수자표법수궤분성ANP조、사리도알조화대조조,매조18지.채용5%우광담산납이담관역행주사방법건립ANP모형.사리도알조우건모후1 h여사리도알200 mS/kg체중관위.술후3、6、12 h분비처사대서,관찰복수량;ELISA법검측혈청TNF-α、IL-6、IL-18수평;류식세포술검측외주혈CD4+、CD8+T세포비례;RT-PCR법검측이선조직TNF-α mRNA표체;면역조화법검측이선조직세포간점부분자1(ICAM-1)단백표체;행이선상규병리검사.결과 술후6 h,대조조적복수량,혈청TNF-α、IL-6、IL-18수평화CD4+、CD8+T 세포비례,이선조직TNF-α mRNA급CAM-1단백표체,병리평분분별위(1.03±0.31)ml、(57.17±11.29)pg/ml、(24.45 ±4.14)pg/ml、(64.23 ±21.85)pg/ml、(47.58±9.21)%、(40.88±2.96)%、0.07±0.02、0.57±0.30、0.67±0.81;ANP조분별위(3.63±0.38)ml、(107.54±33.05)pg/ml、(47.30±11.40)pg/ml、(367.76±108.43)pg/ml、(54.90±7.15)%、(17.17±3.12)%、0.65±0.26、3.20±0.57、11.50±1.87;사리도알조분별위(1.45±0.53)ml、(80.60±20.48)pg/ml、(26.61±10.85)pg/ml、(321.82±85.20)pg/ml、(29.80±2.19)%、(15.52±1.96)%、0.35±0.23、2.37±0.67、8.00±3.03.ANP조제CD8+T세포비례현저강저외,기여지표균교대조조현저증가(P치균<0.05).사리도알조지표균현저저우ANP조(P치균<0.05).결론 사리도알능통과억제TNF-α표체,감소염증체질적석방,종이감경ANP대서적이선병리손해.
Objective To investigate the protective effects of thalidomide on rats with acute necrotizing pancreatitis (ANP) and its mechanism. Methods Fifty four SD rats were randomly divided into the three groups; ANP group, thalidomide group and control group with 18 rats in each group. The model of ANP was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. Rats in thalidomide group received thalidomide 200 mg/kg body weight gastric lavage 1 h after ANP induction. The rats were sacrificed 3 h, 6 h, and 12 h after ANP induction, and the amount of intraperitoneal ascites was quantified. The serum levels of TNF-α, IL-6, IL-18 were measured by EUSA. The proportion of CD4 + T cell, CD8 + T cell in peripheral blood was determined by flow cytometry. The expression of TNF-α mRNA in pancreatic tissue were measured by RT-PCR. The expression of ICAM-1 protein in pancreatic tissue was measured by immunohistochemistry. Pancreatic tissue underwent pathologic examination. Results Six hours after surgery, the amount of ascite, serum levels of TNF-α, IL-6, IL-18, CD4 + T cell, CD,+ T cell, pancreatic TNF-α mRNA and ICAM-1 protein expression, pathologic score in control group was (1.03 ±0.31)ml,(57.17±11.29)pg/ml, (24.45 ±4.14)pg/ml, (64.23 ±21.85)pg/ml, (47.58 ±9.21)% , (40.88 ± 2.96)%, 0.07 ±0.02, 0.57 ±0.30, 0.67 ±0.81, respectively, and the corresponding values were (3.63 ± 0.38)ml, (107.54 ±33.05) pg/ml, (47.30 ± 11.40) pg/ml, (367.76 ± 108.43 ) pg/ml, (54.90 ± 7.15)%, (17.17 ±3.12)%, 0.65 ±0.26, 3.20 ±0.57, 11.50 ±1.87 in ANP group; and (1.45 ±0.53)ml, (80.60 ±20.48) pg/ml, (26.61 ±10.85) pg/ml, (321.82 ±85.20) pg/ml, (29.80 ±2.19)% , (15.52± 1.96)%, 0.35 ±0.23, 2.37 ±0.67, 8.00 ±3.03. Besides the value of CD8 + T cell was significantly decreased, all other values were significantly increased when compared with control group (P <0.05). Conclusions Thalidomide can decrease the release of inflammatory mediator, and reduce the pathological damage of pancreas of ANP rats by inhibiting TNF-α mRNA expression.
