Experimental Study on Expression and Significance of Myeloid Differentiation Factor 88 in Pancreas for Severe Acute Pancreatitis_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

 张梦泽 ,  葛春林 , 张雨京

;

Corresponding author：

葛春林, Email: gechunlin@139.com

Keywords：

重症急性胰腺炎; 髓样细胞分化蛋白88; 核因子-κB

DOI：

10.7507/1007-9424.20140080

Video：

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Abstract Full text Figures/Tables Video References Cited by

目的探讨髓样细胞分化蛋白88（MyD88）在重症急性胰腺炎（SAP）发病机理的作用。方法将48只小鼠按随机数字表法随机分为SAP组（32只）与正常对照组（16只）；再将2组小鼠随机（随机数字表法）分为6、12、24及48 h组，SAP组各亚组每组8只，正常对照组每亚组4只。SAP组小鼠腹腔注射20% L-精氨酸以诱导SAP模型，正常对照组小鼠仅腹腔注射生理盐水。分别于建模术后6、12、24及48 h处死小鼠，取其动脉血，采用ELISA方法检测血清中白细胞介素-1β（IL-1β）、白细胞介素-10（IL-10）及肿瘤坏死因子-α（TNF-α）浓度；同时取其胰腺组织（正常对照组仅术后6 h取材），用逆转录-聚合酶链反应（RT-PCR）方法检测胰腺组织中MyD88 mRNA和核因子-κB（NF-κB）mRNA的表达水平，并进行HE染色。结果镜下见SAP组小鼠的胰腺组织随时间进展其炎症逐渐加重。各时点SAP组小鼠的IL-1β、IL-10及TNF-α浓度均高于正常对照组（P＜0.05）；各时点SAP组与正常对照组（6 h组）相比较，其胰腺组织中MyD88 mRNA及NF-κB mRNA的表达水平均较高（P＜0.05）。各时点SAP组小鼠MyD88 mRNA的表达水平与血清IL-1β、IL-10及TNF-α的浓度和NF-κB mRNA的表达水平均呈正相关（P＜0.01）。结论 MyD88的表达对SAP的发生和发展可能均具有重要的作用。

Citation： 张梦泽, 葛春林, 张雨京. Experimental Study on Expression and Significance of Myeloid Differentiation Factor 88 in Pancreas for Severe Acute Pancreatitis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2014, 21(3): 345-348. doi: 10.7507/1007-9424.20140080 Copy

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12.	Jin B, Sun T, Yu XH, et al. The effects of TLR activation on T-cell development and differentiation[J]. Clin Dev Immunol, 2012, 2012:836485.
13.	Kawai T, Akira S. TLR signaling[J]. Semin Immunol, 2007, 19(1):24-32.
14.	章烈, 李园, 周总光.髓样分化因子88的研究进展:把握TLR信号通路中的瓶颈[J].中国普外基础与临床杂志, 2013, 12(6):685-690.
15.	Neuhöfer P, Liang S, Einwächter H, et al. Deletion of IκBαacti-vates RelA to reduce acute pancreatitis in mice through up-regulation of Spi2A[J]. Gastroenterology, 2013, 144(1):192-201.

1. Ding JL, Zhou ZG, Zhou XY, et al. Attenuation of acute pancr-eatitis by peroxisome proliferator-activated receptor-αin rats:the effect on Toll-like receptor signaling pathways[J]. Pancreas, 2013, 42(1):114-122.
2. Koike Y, Kanai T, Saeki K, et al. MyD88-dependent interleukin-10 production from regulatory CD11b+ Gr-1(high) cells suppresses development of acute cerulein pancreatitis in mice[J]. Immunol Lett, 2012, 148(2):172-177.
3. 徐延钧, 吴新民, 郭亚民.肿瘤坏死因子-α及白介素在急性胰腺炎中的作用[J].中国普外基础与临床杂志, 2010, 17(9):993-996.
4. 李晓晶, 刘瑾.实验动物采血方式优缺点比较[J].辽宁中医药大学学报, 2009, 11(11):217-218.
5. Granger J, Remick D. Acute pancreatitis:models, markers, and mediators[J]. Shock, 2005, 24(Suppl 1):45-51.
6. Carvalho KM, Morais TC, de Melo TS, et al. The natural flavonoid quercetin ameliorates cerulein-induced acute pancreatitis in mice[J]. Biol Pharm Bull, 2010, 33(9):1534-1539.
7. Zhang XP, Zhang L, Chen LJ, et al. Influence of dexamethasone on inflammatory mediators and NF-kappaB expression in multiple organs of rats with severe acute pancreatitis[J]. World J Gastroenterol, 2007, 13(4):548-556.
8. Richer MJ, Lavallée DJ, Shanina I, et al. Toll-like receptor 3 signaling on macrophages is required for survival following coxsac-kievirus B4 infection[J]. PLoS One, 2009, 4(1):e4127.
9. Sharif R, Dawra R, Wasiluk K, et al. Impact of toll-like receptor 4 on the severity of acute pancreatitis and pancreatitis-associated lung injury in mice[J]. Gut, 2009, 58(6):813-819.
10. Hoque R, Sohail M, Malik A, et al. TLR9 and the NLRP3 infla-mmasome link acinar cell death with inflammation in acute panc-reatitis[J]. Gastroenterology, 2011, 141(1):358-369.
11. Tamizhselvi R, Shrivastava P, Koh YH, et al. Preprotachykinin-A gene deletion regulates hydrogen sulfide-induced toll-like receptor 4 signaling pathway in cerulein-treated pancreatic acinar cells[J]. Pancreas, 2011, 40(3):444-452.
12. Jin B, Sun T, Yu XH, et al. The effects of TLR activation on T-cell development and differentiation[J]. Clin Dev Immunol, 2012, 2012:836485.
13. Kawai T, Akira S. TLR signaling[J]. Semin Immunol, 2007, 19(1):24-32.
14. 章烈, 李园, 周总光.髓样分化因子88的研究进展:把握TLR信号通路中的瓶颈[J].中国普外基础与临床杂志, 2013, 12(6):685-690.
15. Neuhöfer P, Liang S, Einwächter H, et al. Deletion of IκBαacti-vates RelA to reduce acute pancreatitis in mice through up-regulation of Spi2A[J]. Gastroenterology, 2013, 144(1):192-201.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Experimental Study on Expression and Significance of Myeloid Differentiation Factor 88 in Pancreas for Severe Acute Pancreatitis

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