抗细胞因子疗法治疗实验性急性坏死性胰腺炎

Effects of anti-inflammatory cytokine in rat acute necrotic pancreatitis model

目的:观察实验性急性坏死性胰腺炎(acutenecroticpancreatitis,ANP)中炎症细胞因子(TNF-α和IL-1β)和抗炎细胞因子TGF-β之间的动态变化;并且分别进行抗TNF-α和抗IL-1β处理,进而探讨对细胞因子产生水平的影响。方法:制作ANP鼠模型,施加抗TNF-α或抗IL-1β处理,制备血清,ELISA检测TNF-α、IL-1β和TGF-β的表达水平。结果:ANP模型中,TNF-α和IL-1β早期(3h)即显著升高,TGF-β进展期(6h)显著升高;TNF-α和IL-1β互相促进分泌;TNF-α单抗处理抑制晚期TGF-β(12h)的产生;IL-1β单抗处理则促进早期(3h)和进展期(6h和9h)TGF-β的产生。结论:ANP的发生发展与TNF-α、IL-1β和TGF-β关系密切,且TNF-α、IL-1β和TGF-β3种细胞因子之间存在动态调节。

Objective： To observe the level of TNF-α, IL-1βand anti-inflammation cytokine TGF-β in the acute necrotic panereatitis （ANP） model before and after anti-TNF-α and anti-IL-1β treatment. Methods： The rat ANP model was constructed, and then the anti-TN F-α antibody and anti-IL-1β antibody was administrated. ELISA was then applied to cheek the serum concentration of TNF-α and IL-1β and TGF-β. Results： The level of TNF-α and IL-1β were increased in early ANP （3 h）, while TGF-β was increased until 6 h after the model construction. TNF-αand IL-1β boosted the secretion of each other. Anti-TNF-α antibody inhibited the production of TGF-β at 12 h, while anti-IL-1β antibody aggravated the secretion of TGF-β at 3 h and 6 h. Conclusion： The pathogenesis of ANP is closely related with TNF-α, IL-α and TGF-1βand the three cytokines regulate each other.