3-N-butylphthalide inhibits neuronal apoptosis in rats with cerebral infarction via targeting P38/MAPK

W. Liao, Y. Zhong, W. Cheng, L.-F. Dong

Department of Neurosurgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou, China. chengweipz@163.com

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• Geriatrics

OBJECTIVE: To study the effect of 3-n-butylphthalide (NBP) on neuronal apoptosis in rats with cerebral infarction (CI) through the p38/mitogen-activated protein kinase (MAPK) pathway.

MATERIALS AND METHODS: A total of 30 rats were divided into control group (healthy rats, n=10), model group (CI rat model, n=10), and NBP group (CI rat model + intraperitoneal injection of NBP, n=10). Then, the neurological function, degree of cerebral ischemia, apoptosis of brain tissues, the protein and messenger ribonucleic acid (mRNA) expressions of p-p38 and MAPK in brain tissues were detected using the neurological score, 2,3,5-triphenyltetrazolium chloride (TTC) staining, Reverse Transcription-Polymerase Chain Reaction (RT-PCR), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and Western blotting, respectively.

RESULTS: In NBP group, the neurological score was significantly lower than in model group, and the difference was statistically significant (p<0.05). The results of TTC staining revealed that the area of the white region in brain slices was significantly larger in model group than in control group, indicating the successful establishment of middle cerebral artery occlusion (MCAO) model. Compared with model group, NBP group had a smaller area and lighter color of the white region in brain slices, suggesting that NBP markedly reduces the MCAO-induced CI. The apoptosis rate in NBP group was higher than in control group (p<0.05), but lower than in model group (p<0.05), while it was higher in model group than in control group (p<0.05). The protein expressions of p38 and MAPK in NBP group were higher than in control group (p<0.05), but lower than in model group (p<0.05), while they were higher in model group than in control group (p<0.05). Moreover, the mRNA expressions of p38 and MAPK were lower in control group than in model group (p<0.05), while they were higher in model group than in NBP group (p<0.05), but there was no significant difference in the mRNA expression of p38 between NBP group and control group (p>0.05).

CONCLUSIONS: NBP alleviates neuronal apoptosis in CI by down-regulating the p38 signal and inhibiting the expression of MAPK, thereby treating CI.

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