›› 2012, Vol. 32 ›› Issue (4): 452-.doi: 10.3969/j.issn.1674-8115.2012.04.018

• Original article (Basic research) • Previous Articles     Next Articles

Effects of lipolysaccharide on expression of ACE and ACE2 in rat pulmonary microvascular endothelial cells and intervention effects of angiotensin-converting enzyme inhibitor

LI Ya-chun, LI Ying-chuan, ZHOU Ming, JIANG Wei   

  1. Department of Anesthesiology, the Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200032, China
  • Online:2012-04-28 Published:2012-04-27
  • Supported by:

    Shanghai Municipal Health Bureau Foundation, 2009089

Abstract:

Objective To investigate the effects of lipolysaccharide (LPS) on expression of angiotensin-converting enzyme (ACE) and angiotensin-converting enzyme 2 (ACE2) in rat pulmonary microvascular endothelial cells (PMVECs) and the intervention effects of angiotensin-converting enzyme inhibitor (ACEI) Captopril. Methods Rat PMVECs were cultured in vitro with tissue explants adherant method, the toxic effects of LPS on PMVECs were investigated by treatment of PMVECs with different concentrations of LPS for different time, and the intervention effects of Captopril were observed. PMVECs were randomly divided into control group (without intervention, n=6), Captopril group (treatment with 10-5 mol/L Captopril for 8 h, n=6), LPS group (treatment with 1 mg/mL LPS for 8 h, n=6) and Captoril+LPS group (treatment with 10-5 mol/L Captopril for 30 min and 1 mg/mL LPS for 8 h, n=6). Cell viability was determined by CCK8, and the expression of ACE and ACE2 in each group was detected by Western blotting. Results LPS had significant toxic effect on rat PMECs, increased the expression of ACE, decreased the expression of ACE2. Captopril significantly inhibited the toxic effects of LPS, reversed the expression of ACE and ACE2, and regulated the level  of ACE and ACE2 to the level of control group. Conclusion ACEI could attenuate the toxic effects of LPS on PMVECs, and the expression of ACE and ACE2 may be involved in the mechanism.

Key words: angiotensin-converting enzyme, angiotensin-converting enzyme inhibitor, rat pulmonary microvascular endothelial cell, acute lung injury, lipolysaccharide