bjectiveTo observe the effecacy of immunosuppressive agents on modulation of the disorders of inflammatory and antiinflammatory cytokines in acute pancreatitis, and to investigate the mechanism of treatment of acute pancreatitis with immunosuppressive agents. MethodsSD male rats were divided into 6 groups: group 1, the normal control group (n=6); group 2, acute pancreatitis induced by ductual injection of 5%sodium cholate sulfur at the volume of 1.0 ml/kg without treatment (n=8). After the pancreatitis were induced, the rest rats were injected intravenously with 5Fu 40 mg/kg (group 3, n=6); or methylprednisolone 30 mg/kg (group 4, n=6); or cyclophosphamide 20 mg/kg (group 5, n=6); or methotrexate 1.2 mg/kg (group 6, n=6). Twentyfour hours afteroperation, the animals were killed, the blood samples were taken for measurement of TNFα, IL1, IL6 (by bioassay), and IL10, TGFβ (by ELISA) as well as amylase. ResultsThe inflammatory cytokines (TNFα,IL1,IL6 ) and the antiinflammatory cytokines (IL10 and TGFβ), in blood of acute pancreatitis were increased significantly. After treated with immunosuppressive agents, both the inflammatory and antiinflammatory cytokines were decreased in different degrees. Some indexes of the severity of acute pancreatitis, such as amylase and pancreatic weight were improved obviously.ConclusionImmunosuppressive agents can regulate inflammatoryassociated cytokines increased remarkably in the acute pancreatitis. Therefore, improvement of acute pancreatitis can be achieved through rectifying the abnormal immunity and relieving the pathophysiological disorders of the acute pancreatitis by immunosuppressive agents.
Citation：
CHEN Xiaoli,HUANG Xinglan,WU Hao,et al.. Modulation of Disorder of InflammatoryAssociated Cytokines with ImmunoSuppressive Agents in Acute Pancreatitis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2002, 9(6): 384-387. doi:
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- 2. McKay CJ, Gallagher H, Brooks B, et al. Increased monocyte cytokine production in association with systemic complications in acute pancreatitis [Ｊ]. Br J Surg， 1996; 83(7)∶919.
- 3. de Beaux AC, Goldie AS, Ross JA, et al. Serum concentrations of inflammatory mediators related to organ failure in patients with acute pancreatitis [Ｊ]. Br J Surg， 1996; 83(3)∶349.
- 4. 崔润林. 5Fu治疗急性胰腺炎的初步观察 [Ｊ]. 实用内科杂志， 1983； 3（5）∶246.
- 5. 谭下宇 . 5氟尿嘧啶配合腹腔引流治疗急性胰腺炎的初步体会 [Ｊ]. 中华医学杂志, 1985； 65（12）∶757.
- 6. Saarrio IA. 5fluorouracil in the treatment of acute pancreatitis [Ｊ]. Am J Surg,1983; 145(3)∶349.
- 7. Kimura K,Shimosegawa T,Sasano H，et al.Endogenous glucocorticoids decrease the acinar cell sensitivity to apoptosis during cerulein pancreatitis in rats [Ｊ].Gastroenterology,1998; 114(2)∶372.
- 8. Darville T， Giroir B， Jacobs R. The systemic inflammatory response syndrome (SIRS): immunology and potential immunotherapy [Ｊ]. Infection, 1993; 21(5)∶279.
- 9. Schlag G, Redl H. Mediators of injury and inflammation [Ｊ]. World J Surg,1996； 20(4)∶406.
- 10. Dinarello CA， Gelfand JA， Wolff SM. Anticytokine strategies in the treatment of the systemic inflammatory response syndrome [Ｊ]. JAMA,1993; 269(14)∶1829.
- 11. Iwagaki H，Hizuta A， Uomoto M，et al. Clinical value of cytokine antagonists in infectious complications [Ｊ].Res Commun Mol Pathol Pharmacol, 1997； 96(1)∶25.
- 12. Artels H, Zantl N, Holzmann B, et al. Special therapeutic approaches for interrupting the cascadefrom SIRS to MOF [Ｊ]. Langenbecks Arch Chir Suppl Kongressbd, 1988; 115∶615.
