云南白药对自发性高血压大鼠肾脏炎症状态的改善作用

Anti-inflammatory Effects of YunNanBaiYao on Kidney of Spontaneously Hypertensive Rat

目的观察云南白药(YNBY)对自发性高血压大鼠(SHR)肾脏炎症状态的影响,探讨其对高血压肾脏疾病的防治作用及机制。方法将6周龄SHR分为YNBY治疗组和高血压模型对照组,在3个时间点(给药6周,给药14周,停药后9周)研究YNBY对SHR血压值、肾脏炎性因子表达和氧化应激水平的影响。结果YNBY对SHR无明显降压作用(P>0.05)。YNBY在mRNA和蛋白水平抑制了细胞间粘附分子-1(ICAM-1)和内皮型一氧化氮合酶(eNOS)在SHR肾脏的高表达(P<0.05)。YNBY在给药14周和停药9周时降低了过氧化物酶体增殖物活化受体γ(PPARγ)的mRNA表达(P<0.05),在给药14周时明显降低了PPARγ的蛋白表达(P<0.05)。YNBY给药后显著降低了SHR肾脏组织蛋白羰基化水平(P<0.05),在给药14周及停药9周后均可显著提高SHR肾脏总抗氧化能力(P<0.05)。结论YNBY给药后能够显著减轻SHR肾脏炎症反应和氧化应激水平,YNBY可能在防治高血压肾病方面具有一定的疗效。

Objective To investigate the effects of YunNanBaiYao （YNBY）on inflammatory status of the kidney from spontaneously hypertensive rats （ SHR）, and to explore preventive and therapeutic usage of YNBY on hypertensive nephropathy. Methods 6 weeks old SHR were divided into SHR control group and SHR - YNBY group. The effects of YNBY on systolic blood pressure, expression of inflammation - related factors and level of oxidative stress were determined at 3 time points ： 6 weeks of YNBY treatment; 14 weeks of YNBY treatment; and 9 weeks post - YNBY treatment. Results YNBY did not affect the elevation of blood pressure of SHR（ P 〉 0.05 ）. However, the TCM compound inhibited the expression of intercellular adhesion molecule - 1 （ ICAM - 1 ） and endothelial nitric oxide synthase （eNOS） at both mRNA and protein levels （P 〈 0.05）. At the time points of 14 weeks of treatment and 9 weeks post - treatment, HMP significantly attenuated peroxisome proliferator - activated receptor γ （PPARγ） mRNA expression （P 〈 0.05）. The protein level of PPARγ was also inhibited by YNBY markedly after 14 weeks of treatment （P 〈 0.05 ）. YNBY significantly reduced protein carbonyl contents of SHR kidney （ P 〈 0.05 ）. In addition, after 14 weeks of treatment, YNBY increased total anti - oxidant capacity of renal tissue from SHR （P 〈 0.05） and this elevated anti - oxidant capacity was even maintained for 9 weeks after treatment （P 〈 0.05 ）. Conclusion YNBY can reduce the inflammatory status and oxidative stress of SHR kidney, which may serve as the base for the advanced therapeutic utility of YNBY in hypertensive renal disease.