铁皮石斛水溶性总蛋白对大鼠胃黏膜损伤及炎症反应的保护机制研究

Study on Protective Mechanisms of Water-soluble Total Protein of Dendrobium candidum on Gastric Mucosal Injury and Inflammatory Response in Rats

研究铁皮石斛水溶性总蛋白对阿司匹林诱导大鼠胃黏膜损伤导致炎症的保护作用及相关机制。将Wistar大鼠随机分为空白对照组、模型组、给药组。给药组灌胃铁皮石斛水溶性总蛋白(10、20 mg/kg)和奥美拉唑(3 mg/kg),5 d后灌胃阿司匹林300 mg/kg建立胃黏膜损伤模型。5 h后处死大鼠,测定胃黏膜损伤程度,血清中前列腺素E2(prostaglandin E2,PGE2)、白介素-1β(interleukin-1β,IL-1β)、白介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)的含量;胃组织中环氧化酶-2 (cyclooxygenase-2,COX-2)、IL-1β、IL-6、TNF-αmRNA以及COX-2、细胞外调节蛋白激酶(extracellular regulated protein kinases,Erk1/2)蛋白的表达。结果显示,铁皮石斛水溶性总蛋白能够有效降低阿司匹林造成的胃黏膜出血及糜烂,且能够使血清中PGE2、SOD含量有明显增加(p<0.01),IL-6、IL-1β、TNF-α、MDA含量明显减少(p<0.01),胃组织中COX-2、IL-1β、IL-6、TNF-αmRNA的表达量以及COX-2、pErk1/2与Erk1/2蛋白表达量的比值均有明显下调(p<0.01)。

The protective effect and related mechanism of water-soluble total protein of Dendrobium candidum on inflammation induced by aspirin in rats with gastric mucosal injury was studied. Wistar rats were randomly divided into a blank control group,a model group,and a drug-administration group. The drug-administered group was given water-soluble total protein(10 mg/kg,20 mg/kg)and omeprazole(3 mg/kg),and the gastric mucosal injury model was established after 5 days of aspirin 300 mg/kg. After 5 h,the rats were sacrificed and the degree of gastric mucosal injury was determined. Serum prostaglandin E2(PGE2),interleukin-1β (IL-1β),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD),malondialdehyde(MDA)content;cyclooxygenase-2(COX-2)in gastric tissue,IL-1β,IL-6,TNF-α mRNA,and expression of COX-2,extracellular regulated protein kinases(Erk1/2)protein.The results showed that the water-soluble total protein of Dendrobium candidum could effectively reduce the gastric mucosal hemorrhage and erosion caused by aspirin,and could significantly increase the content of PGE2 and SOD in serum(p<0.01).The levels of IL-6,IL-1β,TNF-α and MDA were significantly decreased(p<0.01).The expression levels of COX-2,IL-1β,IL-6 and TNF-α mRNA in gastric tissues and the protein expression levels of COX-2 and pErk1/2/Erk1/2 were significantly down-regulated(p<0.01).