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Atorvastatin ameliorates cerebral vasospasm and early brain injury after subarachnoid hemorrhage and inhibits caspase-dependent apoptosis pathway.

Cheng G, Wei L, Zhi-Dan S, Shi-Guang Z, Xiang-Zhen L - BMC Neurosci (2009)

Bottom Line: Hydroxymethylglutaryl coenzyme A reductase inhibitors, also known as statins, has the neuroprotective effects and ameliorating CVS after SAH.TUNEL-positive cells were reduced markedly both in basilar artery and in brain cortex by atorvastatin.The neuroprotective effects of atorvastatin after SAH may be related to its inhibition of caspase-dependent proapoptotic pathway based on the present results.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, PR China. doctorgaocheng@yahoo.com.cn

ABSTRACT

Background: Cerebral vasospasm (CVS) and early brain injury remain major causes of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). Hydroxymethylglutaryl coenzyme A reductase inhibitors, also known as statins, has the neuroprotective effects and ameliorating CVS after SAH. This study was designed to explore apoptosis inhibiting effects of atorvastatin and its potential apoptotic signal pathway after SAH.

Results: Preserving blood-brain-barrier permeability, decreasing brain edema, increasing neurological scores and ameliorating cerebral vasospasm were obtained after prophylactic use of atorvastatin. TUNEL-positive cells were reduced markedly both in basilar artery and in brain cortex by atorvastatin. Apoptosis-related proteins P53, AIF and Cytochrome C were up-regulated after SAH, while they were not affected by atorvastatin. In addition, up-regulation of caspase-3 and caspase-8 after SAH was decreased by atorvastatin treatment both in mRNA and in protein levels.

Conclusion: The neuroprotective effects of atorvastatin after SAH may be related to its inhibition of caspase-dependent proapoptotic pathway based on the present results.

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Related in: MedlinePlus

Cell death assay of DNA-fragmentation after SAH. The results showed that apoptotic-related DNA-fragmentation was increased significantly in SAH rats compared with that in SC rats at 24 hour in basal cortex. Atorvastatin decreased the DNA-fragmentation markedly (*, P < 0.05 vs DMSO group).
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Figure 2: Cell death assay of DNA-fragmentation after SAH. The results showed that apoptotic-related DNA-fragmentation was increased significantly in SAH rats compared with that in SC rats at 24 hour in basal cortex. Atorvastatin decreased the DNA-fragmentation markedly (*, P < 0.05 vs DMSO group).

Mentions: To investigate apoptotic cell death in acute brain injury after SAH, DNA fragmentation was analyzed with a commercial enzyme immunoassay (cell death assay). In the SAH group, the cell death assay revealed that DNA fragmentation was significantly increased at 24 hour compared with the sham operated rats. DNA fragmentation was significantly decreased in atorvastatin-treated rats compared with that in the vehicle-treated rats at the same time point (Figure 2).


Atorvastatin ameliorates cerebral vasospasm and early brain injury after subarachnoid hemorrhage and inhibits caspase-dependent apoptosis pathway.

Cheng G, Wei L, Zhi-Dan S, Shi-Guang Z, Xiang-Zhen L - BMC Neurosci (2009)

Cell death assay of DNA-fragmentation after SAH. The results showed that apoptotic-related DNA-fragmentation was increased significantly in SAH rats compared with that in SC rats at 24 hour in basal cortex. Atorvastatin decreased the DNA-fragmentation markedly (*, P < 0.05 vs DMSO group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2651177&req=5

Figure 2: Cell death assay of DNA-fragmentation after SAH. The results showed that apoptotic-related DNA-fragmentation was increased significantly in SAH rats compared with that in SC rats at 24 hour in basal cortex. Atorvastatin decreased the DNA-fragmentation markedly (*, P < 0.05 vs DMSO group).
Mentions: To investigate apoptotic cell death in acute brain injury after SAH, DNA fragmentation was analyzed with a commercial enzyme immunoassay (cell death assay). In the SAH group, the cell death assay revealed that DNA fragmentation was significantly increased at 24 hour compared with the sham operated rats. DNA fragmentation was significantly decreased in atorvastatin-treated rats compared with that in the vehicle-treated rats at the same time point (Figure 2).

Bottom Line: Hydroxymethylglutaryl coenzyme A reductase inhibitors, also known as statins, has the neuroprotective effects and ameliorating CVS after SAH.TUNEL-positive cells were reduced markedly both in basilar artery and in brain cortex by atorvastatin.The neuroprotective effects of atorvastatin after SAH may be related to its inhibition of caspase-dependent proapoptotic pathway based on the present results.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, PR China. doctorgaocheng@yahoo.com.cn

ABSTRACT

Background: Cerebral vasospasm (CVS) and early brain injury remain major causes of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). Hydroxymethylglutaryl coenzyme A reductase inhibitors, also known as statins, has the neuroprotective effects and ameliorating CVS after SAH. This study was designed to explore apoptosis inhibiting effects of atorvastatin and its potential apoptotic signal pathway after SAH.

Results: Preserving blood-brain-barrier permeability, decreasing brain edema, increasing neurological scores and ameliorating cerebral vasospasm were obtained after prophylactic use of atorvastatin. TUNEL-positive cells were reduced markedly both in basilar artery and in brain cortex by atorvastatin. Apoptosis-related proteins P53, AIF and Cytochrome C were up-regulated after SAH, while they were not affected by atorvastatin. In addition, up-regulation of caspase-3 and caspase-8 after SAH was decreased by atorvastatin treatment both in mRNA and in protein levels.

Conclusion: The neuroprotective effects of atorvastatin after SAH may be related to its inhibition of caspase-dependent proapoptotic pathway based on the present results.

Show MeSH
Related in: MedlinePlus