Sang-qi Granula Reduces Blood Pressure and Myocardial Fibrosis by Suppressing Inflammatory Responses Associated with the Peroxisome Proliferator-Activated Receptors and Nuclear Factor κB Protein in Spontaneously Hypertensive Rats

نویسندگان

  • Lan-Yu Chen
  • Chun-Shui Pan
  • Xiao-Hong Wei
  • Lin Li
  • Jing-Yan Han
  • Li Huang
چکیده

Aim. Sang-qi Granula (SQ) is a compound prepared from Chinese herbs and is currently used for treatment of hypertension in China. Given its protective effects on cardial function in decreasing blood pressure, we investigated the mechanism of protective effects of SQ on myocardium. Methods. 16 male normal Wistar-Kyoto rats and 16 spontaneous hypertension rats (SHR) were employed without medical treatment. 16 SHR were employed with SQ treatment. Rats in each group were sacrificed at two time points (8-week treatment and 16-week treatment). Blood pressure (BP), and heart weight/body weight (HW/BW) were measured. The expression of myeloperoxidase (MCP-1), ICAM-1, TNF- α , and CD68-positive cells was assessed. The interstitial collagen volume fraction (CVF), perivascular collagen volume area (PVCA), and the expression of TGF- β , Smad-3, PPAR α , γ , and NF- κ B (P65 and P50) were observed. Results. SQ significantly inhibited the elevation of the blood pressure and HW/BW of SHR. Next, SQ prevented myocardial fibrosis. Finally, a proinflammatory mediator associated with NF- κ B (TNF- α , ICAM-1, MCP-1, CD68), TGF- β , and Smad-3 related to collagen deposition, which is upregulated in SHR group, was significantly suppressed by SQ. Expression of NF- κ B was decreased in SHQ+SQ group compared to PPAR α , and γ expression was increased by SQ. Conclusion. Treatment with SQ ameliorates cardial fibrosis induced by hypertension by attenuating the upregulation of ICAM-1, TNF- α , MCP-1, TGF- β , Smad-3, P65, and P50 expression and improving PPAR α and PPAR γ expression level. The results suggest that SQ may be an option for preventing cardial fibrosis through PPAR signalling pathway.

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عنوان ژورنال:

دوره 2013  شماره 

صفحات  -

تاریخ انتشار 2013