Yan Wei1, Xinnan Shen, Hui Shen, Jiayi Mai, Min Wu, Guoying Yao. 1. Department of Nutrition and Food Hygiene, School of Public Health, Fudan University, Key Laboratory of Public Health Safety, Ministry of Education, Shanghai 200032, China. 072102107@fudan.edu.cn
Abstract
OBJECTIVE: To study the protective effects of lycopene (LP) on cerebral ischemia-reperfusion injury and oxidative stress in SD rats and the mechanism of them. METHODS: The rats were divided into five groups: normal control group, model control group, sham group and two LP groups (fed with 5 mg/kg bw or 20 mg/kg bw of lycopene daily for 15 days). The model for cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion (MCAO). The score of neurological behavior was evaluated at the 3rd and 24th hours after reperfusion. The rats were put to death 24 h after reperfusion. The size of cerebral infarction was measured. The activities of iNOS, SOD, CAT and the contents of NO and MDA in brain and serum uric acid were measured. The expressions of Bcl-2 mRNA and HIF-1alphamRNA in cortex were examined by using reverse transcription polymerase chain reaction (RT-PCR) technique. RESULTS: In comparison with the model group, the neurological deficits were milder, the volumes of cerebral infarction were smaller, the activities of SOD, CAT in brain tissue were higher, the activities of iNOS as well as the contents of NO, MDA in brain tissue and serum uric acid were lower in Lycopene groups. Compared with the model group and control group, the expression of HIF-1 alpha mRNA of cortex in the high dose lycopene (20 mg/kg bw) group was up-regulated; while the expression of Bcl-2 mRNA of cortex was up-regulated only in the low dose lycopene (5 mg/kg bw) group. CONCLUSION: There were some protective effects of oral administration of lycopene against cerebral ischemia-reperfusion injuries induced by focal cerebral ischemia and oxidative stress. The possible mechanism may be related with increasing activities of antioxidant enzymes, inhibiting lipid peroxidation, decreasing activities of iNOS,and up-regulating the expression of HIF-1alpha mRNA as well as Bcl-2 mRNA.
OBJECTIVE: To study the protective effects of lycopene (LP) on cerebral ischemia-reperfusion injury and oxidative stress in SD rats and the mechanism of them. METHODS: The rats were divided into five groups: normal control group, model control group, sham group and two LP groups (fed with 5 mg/kg bw or 20 mg/kg bw of lycopene daily for 15 days). The model for cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion (MCAO). The score of neurological behavior was evaluated at the 3rd and 24th hours after reperfusion. The rats were put to death 24 h after reperfusion. The size of cerebral infarction was measured. The activities of iNOS, SOD, CAT and the contents of NO and MDA in brain and serum uric acid were measured. The expressions of Bcl-2 mRNA and HIF-1alphamRNA in cortex were examined by using reverse transcription polymerase chain reaction (RT-PCR) technique. RESULTS: In comparison with the model group, the neurological deficits were milder, the volumes of cerebral infarction were smaller, the activities of SOD, CAT in brain tissue were higher, the activities of iNOS as well as the contents of NO, MDA in brain tissue and serum uric acid were lower in Lycopene groups. Compared with the model group and control group, the expression of HIF-1 alpha mRNA of cortex in the high dose lycopene (20 mg/kg bw) group was up-regulated; while the expression of Bcl-2 mRNA of cortex was up-regulated only in the low dose lycopene (5 mg/kg bw) group. CONCLUSION: There were some protective effects of oral administration of lycopene against cerebral ischemia-reperfusion injuries induced by focal cerebral ischemia and oxidative stress. The possible mechanism may be related with increasing activities of antioxidant enzymes, inhibiting lipid peroxidation, decreasing activities of iNOS,and up-regulating the expression of HIF-1alpha mRNA as well as Bcl-2 mRNA.