Apolipoprotein A-I attenuates renal ischemia/reperfusion injury in rats.
Apolipoprotein A-I (ApoA-I), the major protein component of serum high-density lipoprotein (HDL), exhibits its anti-inflammatory activity in inflammatory responses. As renal inflammation plays an important role in ischemia/reperfusion (I/R) injury of the kidney, the aim of this study was to investigate the beneficial effect of ApoA-I on renal I/R injury in rats and the underlined mechanism. Using rats subjected to renal I/R by occlusion of bilateral renal pedicles, we found that administration of ApoA-I significantly reduced serum creatinine levels, serum TNF-alpha and IL-1beta levels as well as tissue myeloperoxidase (MPO) activity, compared with I/R controls. Moreover, ApoA-I treatment suppresses the expression of intercellular adhesion molecules-1 (ICAM-1) and P-selectin on endothelium, thus diminishing neutrophil adherence and the subsequent tissue injury. These results showed that ApoA-I reduced I/R-induced inflammatory responses, decreased renal microscopic damage and improved renal function. It seems likely that ApoA-I protects kidney from I/R injury by inhibiting inflammatory cytokines release and neutrophil infiltration and activation.
Department of Biochemistry, School of Pharmacy, Fudan University, PO Box 257, No. 138 Yixueyuan Road, Shanghai 200032, China.
Ning
N
Shi
Man-Ping
MP
Wu
D000818:Animals; D016632:Apolipoprotein A-I / Q000008:administration & dosage / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D016207:Cytokines / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy; D007674:Kidney Diseases / Q000188:drug therapy*; D018375:Neutrophil Activation / Q000187:drug effects; D020556:Neutrophil Infiltration / Q000187:drug effects; D051381:Rats; D015427:Reperfusion Injury / Q000188:drug therapy*
D016632:Apolipoprotein A-I; D015415:Biomarkers; D016207:Cytokines