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TNF-αI、L-6与高血压肾损害的相关性及其受贝那普利的影响 被引量:17

Tumor necrosis facton alpha and interleukin 6 in hypertensive renal damage and the effects of benazepril on them
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摘要 目的探讨肿瘤坏死因子α(TNF-α)、白介素6(IL-6)与高血压肾损害的关系及其受贝那普利的影响。方法 102例高血压病患者依尿蛋白排泄率(UAER)分为单纯高血压组(n=37)和高血压肾损害组(n=65),再将高血压肾损害者随机分为贝那普利组(n=31)和对照组(n=34)。贝那普利组在其他降压药物的基础上使用贝那普利(10 mg/d),对照组使用除血管紧张素转换酶抑制剂(ACEI)和血管紧张素Ⅱ受体阻滞剂(ARB)以外的降压药物。治疗时间3个月。治疗前后分别测定血清TNF-α、IL-6及UAER。同期选择30例体检健康者作为正常血压组。结果高血压各组血清TNF-α、IL-6水平均高于正常血压组(P<0.05),且高血压肾损害组TNF-α、IL-6水平高于单纯高血压组(P<0.05)。高血压组TNF-α、IL-6水平与UAER成正相关((r=0.79,P<0.01;r=0.75,P<0.01)。对照组治疗后TNF-α显著减低(P<0.05),UAER、IL-6较前降低,但差异无统计学意义(P>0.05),而贝那普利组治疗后UAER、TNF-α、IL-6皆显著降低(P<0.05)。治疗后贝那普利组的UAER、TNF-α、IL-6的降低幅度较对照组显著(P<0.05),而两组的降压幅度无差异(P>0.05)。结论高血压肾损害患者血清TNF-α、IL-6水平明显升高,TNF-α、IL-6可能参与了高血压肾损害的发生和发展;贝那普利显著降低高血压肾损害患者的TNF-α、IL-6及UAER,其作用独立于其降压作用之外。 Objective To study the correlation of TNF-α and IL6 with the hypertensive renal damage and the effects of different antihypertensive drug therapies.Methods 102 patients with essential hypertension were divided into two groups according to their urinary albumin excretion rate(UAER):the hypertensive patients without renal damage(n=37) and the hypertensive patients with renal damage(n=65).The latter was continually assigned randomly to two groups:the study group(n=31) which was treated with benazepril in addition to other antihypertensive drugs,and the control group(n=34) which was treated with regular antihypertensive drugs except angiotensin converting enzyme inhibitors(ACEI) and angiotensin Ⅱreceptor blockers(ARB).Before and after three months of treatment,the blood samples were collected and the serum TNF-α and IL-6 were measured with radioimmune assay.After treatment,the urine samples were collected again for measurement of UAER.Thirty healthy persons were selected as normotensive control group.Results Serum levels of TNF-α and IL-6 were significantly higher in patients with essential hypertension than those in normotensive control group(P0.5),and the hypertensive patients with renal damage had higher levels of TNF-α and IL-6 than the hypertensive patients without renal damage.TNF-α and IL-6 were found to have a positive correlation with UAER(r=0.79,P0.01;r=0.75,P0.01),but no correlation with the level of blood pressure.After treatment,the blood pressure was significantly lowered in both the study group and the control group(P0.05).In control group,after treatment,the level of TNF-α was significantly decreased(P0.05),whilst no statistically significant decrease was found in the levels of IL-6 and UAER(P0.05),despite that the data appeared a tendency towards decrease.Whereas in study group,the levels of UAER,TNFα and IL-6 were all significantly decreased after treatment(P0.05).There was no significant difference in the extent of blood pressure lowering after treatment between the study group and the control group,whereas the extents of the decreases of the levels of UAER,TNF-α and IL-6 in the study group were more than those in control group(P0.05).Conclusion Serum TNF-α and IL-6 are remarkably increased in hypertensive patients and may play an important role in the pathogenesis and development of hypertensive renal damage.ACEIs,Benazepril in this study,can decrease the levels of TNF-α and IL-6,whereby improve,and,to some extent,reverse hypertensive renal damage,independent of their effect of blood pressure lowering.
出处 《中国实验诊断学》 北大核心 2011年第3期492-495,共4页 Chinese Journal of Laboratory Diagnosis
基金 宁夏医科大学研究基金项目(200900)
关键词 高血压肾损害 肿瘤坏死因子Α 白细胞介素6 贝那普利 hypertensive renal damage tumor necrosis factor alpha interleukin 6 benazepril
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  • 1Cotone S, Vadala A, Vella MG. Comparision of tumor necrosis factor and endothelin-1 between essential and renal hypertension patients[J]. J Hum Hypertens, 1998,12(6) :351.
  • 2Dzielak DJ. The immune system and hypertension I J l-Hypertension, 1992, 19,Suppl 1 : I36.
  • 3Simmons EM, Himmelfarb J, Sezer MT, et al. Plasma cytokine levels pre- dict mortality in patients with acute renal failure[J]. Kidney Int, 2004, 65 : 1357.
  • 4Pecoits-Filho R, Barany P, Lindhohn B, et al. Interleukin-6 is an indepen- dent predictor of mortality in patients starting dialysis treatment [ J ]. Nephrol Dial Transplant, 2002,17 : 1684.
  • 5Colutta I, Sold L, Polentamtti N, et al. Selective induction of MCP-1 in human mesmlgial cells by the IL-6/sIL-6R complex [ J ]. Exp Nephrol, 2000,8:37.
  • 6Nanami M, Ookawara T, Otaki Y, et al. Tumor necrosis factor alpha in- duced iron sequestration and oxidative stress in human endothelial cells [ J ~. Atheroscler Thromb Vasc Biol, 2005,25 (12) : 2495.
  • 7Sterzel RB, Schulze-Lohoff E, Marx M, et al. Cytokines and mesangial cells[J]. Kidney Int Suppl, 1993,39:26.
  • 8Ruef C, Budde K, Lacy J, et al. lnterleukin 6 is an autocrine growth factor for mesangial cells [ J ]. Kidney Int, 1990,38 (2) : 249.
  • 9Horii Y, Muraguchi A, Iwano M, et al. Involvement iff IL-6 in Mesangial proliferative glomerulonephrltis~J] .J Inununol, 1989,143(12) :3949.
  • 10Ruiz-Ortega M, Esteban V, Ruperez M, et al. Renal and vascular hyper- tension-induced inflammation: role of angiotensin Ⅱ [J]. Curr Opin Nephrol Hypertens,2C06,15 : 159.

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