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作 者:邱阳[1,2] 杨玉秀[1,2] 任青 王力宁[1,2] 周希静
机构地区:[1]中国医科大学第三临床学院内科 [2]中国医科大学第一临床学院肾内科
出 处:《肾脏病与透析肾移植杂志》1998年第1期22-24,共3页Chinese Journal of Nephrology,Dialysis & Transplantation
摘 要:目的:进一步探明大黄素延缓慢性肾功能衰竭(CRF)进展的机制,观察大黄素对肿瘤坏死因子产生的影响。方法:采用L929细胞生物活性测定法,观察了大黄素和地塞米松对27例CRF患者外周血单个核细胞(PBMC)产生肿瘤坏死因子(TNF)的影响。结果:CRF患者PBMC在有、无脂多糖(LPS)刺激下均较正常对照组产生TNF明显升高,大黄素、地塞米松可显著抑制CRF患者的PBMC产生TNF,呈量效相关关系。结论:PBMC产生TNF增多是CRF患者血浆TNF升高的原因之一,提示CRF患者PBMC处于激活状态。大黄素具有抑制CRF患者PBMC产生TNF的作用。BJECTIVE To study the effect of emodin on the secretion of tumor necrosis factor(TNF) by PBMC in patients with chronic renal failure(CRF).METHODOLOGY We used L929 cell bioactivity assay to determine the in vitro TNF secretion by PBMC,and observed the effects of emodin and dexamethasone on the secretion of TNF in 27 undialyzed CRF patients.RESULTS Bioactivity levels of TNF secreted by PMBC in CRF patietns were higher than that in the healthy controls either with(1387±254 vs 432±091,P<001)or without lipidpolysaccharide(LPS)stimulation (921±185 vs undetectable).No significant difference was found in TNF secretion by PBMC between the uremic and the azotemic patients.Secretion of TNF by PBMC was found to be significantly inhibited by emodin or dexamethason in CRF patients,and a doseeffect correlation was found for the inhibiting effects of emodin and dexamethasone.CONCLUSION The secretion of TNF by PBMC was increased in CRF patients. This may account for the increased plasma level of TNF in CRF patients.It suggested that PBMC in CRF patients might be activated.Emodin and dexamethasone can inhibit the secretion of TNF by PBMC in CRF patients .
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