Effect of lipoxin A4 on inflammatory response in a rat model of permanent focal cerebral ischemia
10.3760/cma.j.issn.0254-1416.2010.07.025
- VernacularTitle:脂氧素A4对大鼠永久性局灶性脑缺血时炎性反应的影响
- Author:
Peipei GUO
;
Yan WU
;
You SHANG
;
Xihong YE
;
Huisheng WU
;
Shiying YUAN
;
Shanglong YAO
- Publication Type:Journal Article
- Keywords:
Lipoxins;
Brain ischemia;
Inflammation
- From:
Chinese Journal of Anesthesiology
2010;30(7):843-846
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of lipoxin A4(LXA4) on inflammatory response in a rat model of permanent focal cerebral ischemia (PFCI). Methods Seventy-two adult male SD rats weighing 200-250 g were randomly divided into 3 groups (n = 24 each):group Ⅰ sham operation (group S); group Ⅱ PFCI and group Ⅲ LXA4. PFCI was induced by thread occlusion of right middle cerebral artery according to the method described by Longa in group Ⅱ and Ⅲ. In group Ⅲ LXA4 100 ng/5 μl was injected into right ventricle of the brain after PFCI was successfully induced, while in group Ⅰ and Ⅱ equal volume of normal saline was injected instead of LXA4. Six animals were killed at 6, 12 and 24 h of ischemia. Their brains were immediately removed for microscopic examination and determination of myeloperoxidase (MPO) activity, TNF-α, IL-10 and transforming growth factor-β1 (TGF-β1) contents in the ischemic cortex. The expression of glial fibrillary acidic protein (GFAP)was measured by immuno-histochemistry. Apoptosis in neurons was assessed using TUNEL. Results PFCI significantly increased MPO activity, TNF-α, IL-10 and TGF-β1 contents and GFAP expression in the ischemic cortex and neuronal apoptosis in group Ⅱ as compared with group S. LXA4 significanfly decreased MPO activity,TNF-α content, GFAP expression and neuronal apoptosis and increased IL-10, TGF-β1 contents at 12,24 h of ischemia. LXA4 significantly ameliorated PFCI-induced cerebral histopathologic damage. Conclusion LXA4 can protect the brain against PFCI injury by inhibiting inflammatory response.
