Inhibition of sodium tanshinone ⅡA sulfonate on the expression of interleukin-6 in anoxia rat models with hypoxic pulmonary hypertension

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Author:
WAN Li-mei(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
LIN Chun-yi(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
CHEN Yu-qin(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
OU Huan-tao(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
ZHAO Lei(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
LU Wen-ju(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
WANG Jian(State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical College, Guangzhou 510120, China)
Journal Title:
Chinese Journal of Biomedical Engineering
Issue:
Volume 18, Issue 03, 2012
DOI:
10.3760/cma.j.issn.1674-1927.2012.03.001
Key Word:
Tanshinone ⅡA sulfonate;Hypertension,pulmonary;Anoxia;Interleukin-6;Models,animal

Abstract: Objective To investigate the impact of sodium tanshinone Ⅱ A sulfonate (STS) on interleukin-6(IL-6) expression in rat models with hypoxic pulmonary hypertension (HPH).Methods The SD rats (n=32) were randomized into normoxic control group (group A),hypoxia model group (group B),low dose ( 10 mg· kg-1 · d-1 )of STS intervention group (group C ) and higb dose (30 mg· kg-1· d-1 )of STS group (group D) (n=8 each).The group A was fed in normoxic cabin,while the rats of group B,C and D were put into the atmospheric hypoxjc cabin,with the oxygen concentration of atmospheric hypoxic cabin being(10± 1)%.On one hand,10 mg/kg and 30 mg/kg STS were intraperitoneally infused into group C and group D at 1 d after hypoxia respectively.On other hand,the same dose of saline was intraperitoneally infused into group A and group B.After successive feeding of 21 d,right ventricular systolic pressure (RVSP) and mean arterial pressure (mPAP) were detected in rats of each group by right cardiac manometric method,the vascular morphology and inflammatory response observed by hematoxylin- eosin (HE) staining,IL- 6 component in serum measured by ELISA,and the IL-6 expression detected by real-time fluorescent quantitative PCR.Results The hypoxia significantly induced the increases of RVSP and mPAP.Nevertheless,the increasing levels of RVSP and mPAP were obviously decreased after intervention of STS.The mPAPs were (12.922±0.442) mm Hg( 1 mm Hg=0.133 kPa),(26.737±2.222) mm Hg,( 19.948±1.681 ) mm Hg and(18.547± 1.090) mm Hg in A,B,C,D groups,and RVSPs were (24.677 ± 1.725) mm Hg,(63.675±5.283) mm Hg,(49.250±3.816) mm Hg and (41.839±3.993) mm Hg respectively.STS could improve the vascular morphology and inflammatory response in rats with HPH.Compared with group B,group C and group D had reduced thickening of small arterial wall and smooth muscle layer,narrowing lumen and less lymphocytes and neutrophil infiltration in peripheral vessels.However,the inflammatory response in group C and group D remained obvious as compared with that in goup A.After hypoxia induction,the IL-6 component in group B was significantly elevated as compared with that in group A (P<0.05).While after intervention of STS,the IL-6 components in group C and group D were lowered as compared with those in group A and group B(all P<0.05),with IL 6 component in group C higher than that in group D(P<0.05).Hypoxia significantly induced the expression of IL-6 mRNA in hung tissues,while STS obviously inhibited the expression of IL-6 mRNA.However,the expression levels in these groups were still higher than that in normoxic control group,with group B> group C> group D> group A (all P<0.05).Conclusion STS is effective in treatment of chronicity HPH caused by hypoxia,which may be correlated with its inhibiting effects on IL-6.

  • [1]吴焕明,尹为华.丹参酮ⅡA硫酸钠对低氧诱导肺血管平滑肌细胞增殖的影响.同济医科大学学报,2001,30:106-108.
  • [2]莫晓能,陈文彬,程德云,等.丹参对慢性低氧大鼠肺动脉压力等的影响.临床肺科杂志,2002,7:1-3.
  • [3]Lam SY,Tipoe GL,Liong EC,et al.Chronic hypoxia upregulates the expression and function of proinflammatory cytokines in the rat carotid body.Histochem Cell Biol,2008,130:549-559.
  • [4]Stenmark KR,Fagan KA,Frid MG.Hypoxia-induced pulmonary vascular rcmodeling:cellular and molecular mechanisms.Circ Res,2006,99:675-691.
  • [5]Steiner MK,Syrkina OL,Kolliputi N,et al.Interleukin-6 overexpression induces pulmonary hypertension.Circ Res,2009,104:236-244,28p-244p.
  • [6]Jang SI,Jeong SI,Kim KJ,et al.Tanshinone IIA from Salvia miltiorrhiza inhibits inducible nitric oxide synthase expression and production of TNF-alpha,1L-lbeta and IL-6 in activated RAW 264.7cells.Planta Med,2003,69:1057-1059.
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