Butylphthalide in the protection of focal cerebral ischerma-reperfusion in rats by enhancing the antioxidant activity

Abstract

Objective To investigate the protective effect of butylphthalide for focal cerebral ischemiareperfusion injury and its possible mechanism. Methods A total of 60 healthy and clean adult Sprague-Dawley rats were randomly divided into sham operation, saline control, low-dose butylphthalide and high-dose butylphthalide groups （n = 15 in each group）. A focal cerebral ischemia-reperfusion model was induced by the suture method. At the beginning of reperfusion, 100 mg/kg and 400 mg/kg butylphthalide injection were injected intraperitoneally in the rats of the low-dose butylphthalide and high-dose butylphthalide groups; 0. 5 ml/kg saline was injected intrapexitoneally in rats of the sham operation and saline control groups. All the rats were sacrificed after 24 h of ischemia-reperfusion. Results The degree of neurological deficit in the low-dose butylphthalide （t = 1. 488, P = 0. 000） and high-dose butylphthalide （t = 2. 362, P = 0. 000） groups were significantly improved compared to the saline control group, in which the high-dose butylphthalide group was improved more significantly than the low-dose butylphthalide ffoup （t= -0. 873, P= 0. 000）. The infarct volume in the low-dose butylphthalide （t = 18. 589, P =0. 000） and high-dose butylphthalide （t =36. 963, P = 0. 000） groups were reduced significantly compared to the saline control group, in which the infarct volume of the high-dose butylphthalide group was reduce more significantly than that of the low-dose butylphthalide group （t = - 18. 374, P =0. 000）. HE staining showed that neurons were sparse, there were a large number of degeneration and necrosis, cell space became larger, and the intercellular substances showed vacuolar changes. In the butylphthalide group, the neuronal degeneration and necrosis reduced significantly, the survival of nerve cells increased, and the improvement of the high-dose butylphthalide group was more remarkable. SOD activity of the low-dose and high-dose butylphthalide groups were increased significantly compared to the sham operation and saline control groups （all P 〈0. 05）, in which the SOD activity in the high-dose butylphthalide group was significantly higher than that in the low-mall dose butylphthalide group （t = 80. 199, P = 0. 000）; The MDA levels in the low-dose and high-dose butylphthalide groups were decreased significantly compared to the sham operation and saline control groups （all P 〈 0. 05）, in which the MDA level in the high-dose butylphthalide group was significantly lower than that in the low-dose butylphthalide group （t = -1. 308, P= 0. 000）. Conclusions The protective effect of butylphthalide on ischemia-reperfusion injury may be associated with the increased antioxidant activity. Key words: Benzofurans; 3-n-butylphthalide; Brain Ischemia; Reperfusion Injury; Superoxide Dismutase; Malondialdehyde; Neuroprotective Agelats; Rats