Premium
Haemin‐enhanced expression of haem oxygenase‐1 stabilizes erythrocyte‐induced vulnerable atherosclerotic plaques
Author(s) -
Lin Hui Li,
Zhang Lei,
Liu Chun Xi,
Xu Xin Sheng,
Tang Meng Xiong,
Lv Hui Xia,
Li Chang Jiang,
Sun Hui Wen,
Zhang Mei,
Hong Jiang,
Zhang Yun
Publication year - 2010
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.00799.x
Subject(s) - saline , adventitia , medicine , inflammation , macrophage , pathology , heme oxygenase , hemin , chemistry , heme , biochemistry , in vitro , enzyme
Background and purpose: Previous studies demonstrated that intraplaque haemorrhage increased the contents of cholesterol and oxidants in atherosclerotic plaques. The present study was aimed to test the hypothesis that enhanced expression of haem oxygenase‐1 (HO‐1) may stabilize vulnerable plaques. Experimental approach: Intravascular ultrasound (IVUS) was performed to identify three similar abdominal aortic plaques in each of 58 fat‐fed New Zealand rabbits after aortic balloon injury. With the guidance of IVUS, 50 µL autologous erythrocytes (RBC) or normal saline (NS) were injected from adventitia into two of the pre‐selected plaques, respectively, whereas the third plaque served as a blank control. All rabbits were randomly divided into two groups, receiving intraperitoneal injection of haemin and saline respectively. Key results: Compared with NS or control plaques, RBC plaques had more macrophage infiltration and lipid content, thinner plaque fibrous cap, and higher expression of inflammatory factors and incidence of plaque rupture. RBC plaques in the haemin group had about a 50% lower incidence of plaque rupture than those in the control group. Conclusions and implications: Haem oxygenase‐1 may eliminate haem or other oxidants, exert unexpected anti‐oxidative and anti‐inflammatory effects and serve as a promising approach to the direct inhibition of erythrocyte‐induced plaque instability.