Protective effects of recombinant SCR15-18 domain of human soluble complement receptor type 1 on myocardial ischemia and reperfusion injury.
- Author:
Bing TAN
1
;
Yang-Jun LAN
;
De-Chun ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Creatine Kinase; metabolism; Disease Models, Animal; Humans; L-Lactate Dehydrogenase; metabolism; Myocardial Reperfusion Injury; metabolism; pathology; prevention & control; Peroxidase; metabolism; Rats; Rats, Sprague-Dawley; Receptors, Complement; therapeutic use; Receptors, Complement 3b; metabolism; Recombinant Proteins; therapeutic use
- From: Chinese Journal of Cardiology 2007;35(11):1037-1040
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of recombinant SCR15-18 domain of human soluble complement receptor type 1 (sCR1-SCR-15-18) in rats underwent myocardial ischemia and reperfusion (I/R).
METHODSSprague-Dawley rats were randomly divided into three groups (n = 12 each group): sham (SO); 30 min ischemia/3h reperfusion (I/R) and I/R plus sCR1-SCR15-18 (15 mg/kg before I/R, sCR1). Serum LDH, CK and cardiac myeloperoxidase (MPO) activity were measured. Infarct size, myocardial histopathological changes and myocardial C3c were also compared among groups.
RESULTSInfarct size [(16.1 +/- 3.3)% vs. (22.9 +/- 3.0)%, infarct zone/left ventricular mass, P < 0. 05] and CK [(2532.5 +/- 597.1) U/L vs. (3400.9 +/- 534.9) U/L, P < 0. 05] and LDH [(5436.2 +/- 611.3) U/L vs. (6572.0 +/- 476.3) U/L, P < 0. 05] as well as MPO activity in infarct zone [(0.81 +/- 0.14) U/g vs. (1.12 +/- 0.13) U/g, P < 0.05] were significantly decreased post sCR1 compared to I/R group. sCR1 also significantly attenuated histological myocardial injury and reduced the deposition of C3c in infarct zone.
CONCLUSIONsCR1-SCR15-18 protein exerts cardioprotective effects in this rat I/R model.
