Journal of Capital Medical University ›› 2010, Vol. 31 ›› Issue (2): 183-186.

• 儿科学专题 • Previous Articles     Next Articles

Impact of Sulfur Dioxide on the Endoplasmic Reticulum Stress of Aortic Smooth Muscle Cells in the Spontaneously Hypertensive Rats

ZHU Lu-lu1, ZHAO Xia1, TANG Chao-shu2,3, DU Jun-bao1,3, JIN Hong-fang1*   

  1. 1. Department of Pediatrics, Peking University First Hospital;2. Department of Physiology and Pathophysiology, Peking University Health Science Center; 3. Key Laboratory of Molecular Cardiovascular Diseases, Ministry of Education
  • Received:1900-01-01 Revised:1900-01-01 Online:2010-04-21 Published:2010-04-21
  • Contact: JIN Hong-fang

Abstract: Objective To explore the effect of sulfur dioxide(SO2) on the endoplasmic reticulum stress(ERS) in the aortic smooth muscle cells of spontaneously hypertensive rat(SHR). Methods Seven male WKY rats were used as WKY control group. Twelve male SHRs at the age of 4 weeks were randomly divided into SHR control group and SHR+SO2 donor(Na2SO3/NaHSO3) group, respectively. Five weeks later, the blood pressure was determined. SO2 content in the plasma was detected by reversephase high performance liquid chromatography with fluorescence detection(HPLC). The expressions of glucose-regulated protein 78(GRP78) and caspase-12 in the aortic smooth muscle cells were measured by immuohistochemistry. Results Compared with WKY control group, SO2 contents in the plasma were decreased, while the blood pressure and the expressions of GRP78 and caspase-12 in the aortic smooth muscle cells were increased in the rats of SHR control group significantly, respectively. Administration of SO2 donor increased the SO2 content in the plasma in the rats of SHR control group. Moreover, SO2 donor decreased the blood pressure and the expressions of GRP78 and caspase-12 in the aortic smooth muscle cells of SHR control rats. Conclusion SO2 might inhibit the activation of ERS in the aortic smooth muscle cells of hypertensive rats.

Key words: sulfur dioxide, hypertension, aortic, endoplasmic reticulum stress

CLC Number: