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：

 張夢澤 ,  葛春林 , 張雨京

;

Corresponding?author：

葛春林, Email: gechunlin@139.com

Keywords：

重癥急性胰腺炎; 髓樣細胞分化蛋白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

目的探討髓樣細胞分化蛋白88（MyD88）在重癥急性胰腺炎（SAP）發病機理的作用。方法將48只小鼠按隨機數字表法隨機分為SAP組（32只）與正常對照組（16只）；再將2組小鼠隨機（隨機數字表法）分為6、12、24及48 h組，SAP組各亞組每組8只，正常對照組每亞組4只。SAP組小鼠腹腔注射20% L-精氨酸以誘導SAP模型，正常對照組小鼠僅腹腔注射生理鹽水。分別于建模術后6、12、24及48 h處死小鼠，取其動脈血，采用ELISA方法檢測血清中白細胞介素-1β（IL-1β）、白細胞介素-10（IL-10）及腫瘤壞死因子-α（TNF-α）濃度；同時取其胰腺組織（正常對照組僅術后6 h取材），用逆轉錄-聚合酶鏈反應（RT-PCR）方法檢測胰腺組織中MyD88 mRNA和核因子-κB（NF-κB）mRNA的表達水平，并進行HE染色。結果鏡下見SAP組小鼠的胰腺組織隨時間進展其炎癥逐漸加重。各時點SAP組小鼠的IL-1β、IL-10及TNF-α濃度均高于正常對照組（P＜0.05）；各時點SAP組與正常對照組（6 h組）相比較，其胰腺組織中MyD88 mRNA及NF-κB mRNA的表達水平均較高（P＜0.05）。各時點SAP組小鼠MyD88 mRNA的表達水平與血清IL-1β、IL-10及TNF-α的濃度和NF-κB mRNA的表達水平均呈正相關（P＜0.01）。結論 MyD88的表達對SAP的發生和發展可能均具有重要的作用。

Citation： 張夢澤, 葛春林, 張雨京. 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

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.	徐延鈞, 吳新民, 郭亞民.腫瘤壞死因子-α及白介素在急性胰腺炎中的作用[J].中國普外基礎與臨床雜志, 2010, 17(9):993-996.
4.	李曉晶, 劉瑾.實驗動物采血方式優缺點比較[J].遼寧中醫藥大學學報, 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, 李園, 周總光.髓樣分化因子88的研究進展:把握TLR信號通路中的瓶頸[J].中國普外基礎與臨床雜志, 2013, 12(6):685-690.
15.	Neuh?fer P, Liang S, Einw?chter 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. 徐延鈞, 吳新民, 郭亞民.腫瘤壞死因子-α及白介素在急性胰腺炎中的作用[J].中國普外基礎與臨床雜志, 2010, 17(9):993-996.
4. 李曉晶, 劉瑾.實驗動物采血方式優缺點比較[J].遼寧中醫藥大學學報, 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, 李園, 周總光.髓樣分化因子88的研究進展:把握TLR信號通路中的瓶頸[J].中國普外基礎與臨床雜志, 2013, 12(6):685-690.
15. Neuh?fer P, Liang S, Einw?chter 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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