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. 2014 Feb 1;9(3):268-75.
doi: 10.4103/1673-5374.128220.

Atorvastatin protects against cerebral ischemia/reperfusion injury through anti-inflammatory and antioxidant effects

Qiuyun Tu  1 , Hui Cao  2 , Wei Zhong  2 , Binrong Ding  1 , Xiangqi Tang  2
Affiliations

Atorvastatin protects against cerebral ischemia/reperfusion injury through anti-inflammatory and antioxidant effects

Qiuyun Tu et al. Neural Regen Res. .

Abstract

In addition to its lipid-lowering effect, atorvastatin exerts anti-inflammatory and antioxidant effects as well. In this study, we hypothesized that atorvastatin could protect against cerebral ischemia/reperfusion injury. The middle cerebral artery ischemia/reperfusion model was established, and atorvastatin, 6.5 mg/kg, was administered by gavage. We found that, after cerebral ischemia/reperfusion injury, levels of the inflammation-related factors E-selectin and myeloperoxidase were upregulated, the oxidative stress-related marker malondialdehyde was increased, and superoxide dismutase activity was decreased in the ischemic cerebral cortex. Atorvastatin pretreatment significantly inhibited these changes. Our findings indicate that atorvastatin protects against cerebral ischemia/reperfusion injury through anti-inflammatory and antioxidant effects.

Keywords: E-selectin; NSFC grant; atorvastatin; blood-brain barrier; brain injury; cerebral ischemia/reperfusion; free radicals; inflammation; malondialdehyde; myeloperoxidase; nerve regeneration; neural regeneration; stroke; superoxide dismutase.

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Conflict of interest statement

Conflicts of interest: None declared.

Figures

Figure 1
Figure 1
Morphology of the rat brain after middle cerebral artery occlusion (triphenyltetrazolium chloride staining). In the sham surgery group (A), sections were uniformly red. In the model group (B), the brain tissue in the infarct area was white (arrow).
Figure 2
Figure 2
Effect of atorvastatin on neurological function in rats with cerebral ischemia/reperfusion (I/R). Data are expressed as mean ± SD of eight rats for each group. aP < 0.05, vs. sham group (0 score) (one-way analysis of variance and least signifi-cant difference test). The higher scores indicate more severe neurologi-cal function deficit. Sham: Sham surgery group.
Figure 3
Figure 3
Effect of atorvastatin on E-selectin expression in the cortex of rats with cerebral ischemia/reperfusion (immunohistochemical staining, × 400). E-selectin-positive cells (arrows) were mainly distributed in the cortex and hippocampus, and E-selectin immunoreactivity was expressed in nerve cells and vascular endothelial cell membranes and cytoplasm. E-selectin expression in the model group (B) and in the atorvastatin group (C) was increased significantly compared with the sham surgery group (A). Compared with the model group, the increase in E-selectin expression was significantly inhibited in the atorvastatin group. The arrows show expression of E-selectin.
Figure 4
Figure 4
Effect of atorvastatin on myeloperoxidase expression in the cortex of rats with cerebral ischemia/reperfusion (immunohistochemical staining, × 400). Myeloperoxidase labeling (arrows) was mainly distributed in the cytoplasm, with minor labeling in the cell membrane. Myeloperoxidase expression in the model and atorvastatin groups was increased significantly compared with the sham surgery group (A). Compared with the model group (B), the increase in myeloperoxidase expression was significantly inhibited in the atorvastatin group (C). Arrows point to labeling for myeloperoxidase.
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