摘要
目的研究酪酸梭菌干预对高尿酸血症大鼠血清尿酸、脂多糖、白介素6、肿瘤坏死因子α的影响。方法将40只SD大鼠随机分为正常对照组、高尿酸模型组、苯溴马隆干预组(3 mg/kg·d)和酪酸杆菌干预组(活菌1.5×107CFU/d),每组10只。除正常对照组外各组给予酵母膏联合氧嗪酸钾灌胃制备高尿酸血症模型,各组药物及活菌每天灌胃1次,连续12周。观察各组大鼠血尿酸、脂多糖、白介素6、肿瘤坏死因子α水平变化。结果实验期间高嘌呤饮食大鼠血尿酸水平较正常对照组明显升高(P<0.01),高尿酸血症模型建立成功且稳定。高尿酸模型组大鼠血脂多糖、白介素6、肿瘤坏死因子α水平与血尿酸水平呈正相关。苯溴马隆及酪酸梭菌干预处理后大鼠血尿酸、脂多糖、白介素6、肿瘤坏死因子α水平有明显下降(P<0.01),干预时间越长,效果越佳,其中苯溴马隆降尿酸效应更为明显,酪酸梭菌下调脂多糖、白介素6、肿瘤坏死因子α等炎性因子作用更为明显(P<0.01)。结论高尿酸血症大鼠可能存在慢性炎症反应,酪酸梭菌可有效降低血尿酸水平,同时抑制炎症细胞因子的生成,维持肠道免疫稳态。
Objective To investigate the effects of intragastric administration of Clostridium butyricum in regulating serum uric acid, lipopolysaccharides(LPS), interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) in rats with hyperuricemia rats.Methods Forty SD rats were randomized into 4 equal groups, namely the normal control group, hyperuricemia model group,benzbromarone(3 mg/kg daily) intervention group and live Clostridium butyricum group(1.5×107CFU/day). Except for those in the control group, the rats were subjected to intragastric administration of yeast extract and oteracil potassium once daily for12 weeks to induce hyperuricemia with corresponding treatments. The changes in serum uric acid, lipopolysaccharides, IL-6and TNF-α in each group were detected. Results The serum level of uric acid was significantly higher in rats fed with highpurine diet than in the control rats(P<0.01), demonstrating the successful establishment of hyperuricemia models. In rats with hyperuricemia, serum uric acid level was positively correlated with the levels of LPS, IL-6 and TNF-α, and their serum levels decreased significantly and progressively with time in Benzbromarone group and Clostridium butyricum group.Benzbromarone was more effective in decreasing serum uric acid in the rats, while Clostridium butyricum produced a stronger effect in down-regulating the inflammatory mediators. Conclusion Chronic inflammatory reaction exists in rats with hyperuricemia. Intragastric administration of Clostridium butyricum can effectively decrease serum uric acid level and inhibit the inflammatory cytokines, and thus contributes to immune homeostasis in the intestines.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2017年第5期678-682,共5页
Journal of Southern Medical University
