Effects of curcumin on the expression of nuclear factor-kappaB and intercellular adhesion molecular 1 in rats with cerebral ischemia-reperfusion injury.
- Author:
Rong ZHUANG
1
;
Meng-Xiang LIN
;
Qiu-Ying SONG
;
Jun LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; metabolism; pathology; Curcumin; pharmacology; Down-Regulation; drug effects; Intercellular Adhesion Molecule-1; genetics; metabolism; Male; NF-kappa B; genetics; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism
- From: Journal of Southern Medical University 2009;29(6):1153-1155
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of curcumin on the expression of nuclear factor-kappaB (NF-kappaB) and intercellular adhesion molecular 1 (ICAM-1) in rats with cerebral ischemia-reperfusion (IR) injury.
METHODSA total of 160 SD rats were randomized equally into sham-operated group, IR model group, curcumin treatment group and solvent control group. Global cerebral ischemia/reperfusion injury was induced in the latter 3 groups with subsequent corresponding treatment. At 6 h and 1, 3, and 7 days after the injury, 10 rats from each group were sacrificed, and brain sections were prepare for HE staining, immunohistochemical staining for NF-kappaB, and enzyme-linked immunosorbent assay for ICAM-1 expression.
RESULTSIn the IR model group, the contour of the pyramidal cells in hippocampal CA1 region was almost indistinguishable after the injury, whereas more than 70% of the pyramidal cells retained distinct cell contour and nuclear boundary in curcumin treatment group. At 6 h and 1, 3, and 7 days after the IR injury, the expression of NF-kappaB in curcumin treatment group showed significantly reduction in comparison with that in the IR model and solvent control groups (P<0.05), and the content of ICAM-1 protein was also reduced, which was especially obvious at 1 and 3 days (P<0.05).
CONCLUSIONCurcumin can ameliorate cerebral pathological changes in the event of IR injury by suppressing the expressions of NF-kappaB and ICAM-1.