摘要
目的探讨表没食子儿茶素没食子酸酯(EGCG)对高尿酸血症大鼠血管内皮炎症因子的作用。方法将36只雄性SD大鼠分为正常对照组、模型对照组、EGCG低剂量组、EGCG中剂量组、EGCG高剂量组、别嘌呤醇组,5周后,运用RT-PCR检测大鼠主动脉MCP-1、TNF-α、ICAM-1、ET-1及e NOS表达量,以及大鼠血清尿酸、肌酐、尿素氮和黄嘌呤氧化酶(XO)水平。结果模型对照组大鼠的血尿酸和XO水平显著高于正常对照组(P<0.01),EGCG各浓度组及别嘌呤醇组大鼠的血尿酸和XO水平与模型对照组相比较则有不同程度下降(P<0.01)。模型对照组大鼠主动脉MCP-1、TNF-α、ICAM-1的mRNA表达量较正常对照组显著升高(P<0.01),EGCG各浓度组和别嘌呤组大鼠主动脉TNF-α、ICAM-1的mRNA表达量与模型对照组相比显著下降(P<0.01),EGCG高剂量组和别嘌呤组MCP-1 mRNA表达量与模型对照组相比显著下降(P<0.05)。EGCG中剂量组和别嘌呤组ET-1 mRNA表达量与模型对照组相比显著下降(P<0.05)。结论 EGCG干预可以降低高尿酸血症大鼠的血尿酸水平,同时减少血管内皮炎症因子的表达。
Aim To explore the effects of epigallocatechin gallate（ EGCG） on the inflammation of vascular endothelium in hyperuricemia rats. Methods Thirty-six male SD rats were divided into normal control group,model control group,EGCG low dose（ EGCG-L） group,EGCG medium dose（ EGCG-M） group,EGCG high dose（ EGCG-H）group and allopurinol group. After five weeks,the expression of MCP-1,TNF-α,ICAM-1,ET-1 and e NOS in hyperuricemia rats were detected by RT-PCR,serum uric acid,creatinine,urea nitrogen and xanthine oxidase（ XO） were determined. Results Compared with normal control group,the levels of serum uric acid and XO were increased in model control group（ P〈0.01）. Compared with model control group,the levels of serum uric acid and XO were significantly decreased in EGCG-L group,EGCG-M group,EGCG-H group and allopurinol group（ P〈0.01）. Compred with normal control group,the mRNA expression of MCP-1,TNF-α and ICAM-1 was markedly increased in model control group（ P〈0.01）. The expression of MCP-1 mRNA in EGCG-H group and allopurinol group was markedly decreased as compared with model control group（ P〈0.05）. Compared with model control group,the expression of TNF-α,ICAM-1 mRNA was significantly decreased in EGCG-L group,EGCG-M group,EGCG-H group and allopurinol group（ P〈0.01）. The mRNA expression of ET-1 in EGCG-M group was also decreased significantly（ P〈0. 01）. Conclusion EGCG attenuated serum uric acid and the inflammation of vascular endothelium in hyperuricemia rats.
出处
《中国动脉硬化杂志》
CAS
北大核心
2017年第1期13-18,共6页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金资助项目(81100603)
