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目的:观察麝香保心丸(HMP)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HMP治疗组和高血压模型对照组,以同周龄的Wistar-Kyoto(WKY)大鼠为正常对照,在3个时间点(给药6周,给药14周,停药9周)研究HMP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:在整个实验过程中HMP对SHR无明显降压作用(P>0.05)。HMP在mRNA和蛋白水平抑制了细胞间粘附分子-1(ICAM-1)和诱导型一氧化氮合酶(iNOS)在SHR肾脏的高表达(P<0.05),在mRNA水平抑制了肿瘤坏死因子-α(TNF-α)的高表达(P<0.05)。HMP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),而在给药6周和给药14周时明显降低了PPARγ的蛋白表达(P<0.05)。HMP给药14周及停药9周后均可显著提高SHR肾脏组织总抗氧化能力(P<0.05),给药14周时能显著降低SHR肾脏组织蛋白羰基化水平(P<0.05)。结论:HMP给药后能够显著减轻SHR肾脏炎症反应,并且伴随着肾脏氧化应激水平的降低,这可能是HMP在防治高血压肾病方面具有应用潜能的作用机理。
Objective: To observe the effect of Shexiang Baoxin Pill (HMP) on renal inflammatory state in spontaneously hypertensive rats (SHR) and to explore its preventive and therapeutic effects on hypertensive renal disease. Methods: Six-week-old SHRs were divided into HMP-treated group and hypertensive model control group. Wistar-Kyoto (WKY) rats of the same age were used as normal control. At 3 time points Week, withdrawal for 9 weeks) to study the effect of HMP on SHR blood pressure, renal inflammatory factor expression and oxidative stress. Results: HMP had no significant antihypertensive effect on SHR during the whole experiment (P> 0.05). HMP inhibited the expression of ICAM-1 and iNOS in SHR kidney at the mRNA and protein levels (P <0.05), and inhibited the tumor necrosis at the mRNA level High expression of factor-α (TNF-α) (P <0.05). HMP decreased mRNA expression of peroxisome proliferator-activated receptor γ (PPARγ) 14 weeks after drug administration and 9 weeks after drug withdrawal (P <0.05), but significantly decreased at 6 weeks and 14 weeks after administration Reduced PPARγ protein expression (P <0.05). HMP administration for 14 weeks and withdrawal for 9 weeks significantly increased SHR renal tissue total antioxidant capacity (P <0.05), and 14-week HMP treatment significantly reduced the protein levels of SHR renal tissue (P <0.05). CONCLUSIONS: HMP administration can significantly reduce the inflammatory response in SHR kidneys, accompanied by decreased oxidative stress in the kidneys, which may be the mechanism of HMP’s potential in preventing and treating hypertensive nephropathy.