Antioxidant Effect of Salvianolic Acid B on Hippocampal CA1 Neurons in Mice with Cerebral Ischemia and Reperfusion Injury
Objetive: TO investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B (Sal B) extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury. Methods: Forty male National Institute of Health (NIH) mice were randomly divi...
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Published in | Chinese journal of integrative medicine Vol. 21; no. 7; pp. 516 - 522 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
Beijing
Chinese Association of Traditional and Western Medicine
01.07.2015
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Subjects | |
Online Access | Get full text |
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Summary: | Objetive: TO investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B (Sal B) extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury. Methods: Forty male National Institute of Health (NIH) mice were randomly divided into 4 groups with 10 animals each, including the sham group, the model group, the SalB group (SalB 22.5 mg/kg) and the nimodipine (Nim) group (Nim 1 mg/kg). A mouse model of cerebral ischemia and reperfusion injury was established by bilateral carotid artery occlusion for 30 rain followed by 24-h reperfusion. The malondialdehyde (MDA) content, the nitric oxide synthase (NOS) activity, the superoxide dismutase (SOD) activity and total anti- oxidant capability (T-AOC) of the pallium were determined by biochemistry methods. The morphologic changes and Bcl-2 and Bax protein expression in hippocampal CA1 neurons were observed by using hematoxylin- eosin staining and immunohistochemistry staining, respectively. Results: In the SalB group, the MDA content and the NOS activity of the pallium in cerebral ischemia-reperfusion mice significantly decreased and the SOD activity and the T-AOC significantly increased, as compared with the model group (P〈0.05 or P〈0.01). The SalB treatment also rescued neuronal loss (P〈0.01) in the hippocampal CA1 region, strongly promoted Bcl-2 protein expression (P〈0.01) and inhibited Bax protein expression (P〈0.05). Conclusions: SalB increases the level of antioxidant substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SalB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SalB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease. |
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Bibliography: | 11-4928/R Objetive: TO investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B (Sal B) extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury. Methods: Forty male National Institute of Health (NIH) mice were randomly divided into 4 groups with 10 animals each, including the sham group, the model group, the SalB group (SalB 22.5 mg/kg) and the nimodipine (Nim) group (Nim 1 mg/kg). A mouse model of cerebral ischemia and reperfusion injury was established by bilateral carotid artery occlusion for 30 rain followed by 24-h reperfusion. The malondialdehyde (MDA) content, the nitric oxide synthase (NOS) activity, the superoxide dismutase (SOD) activity and total anti- oxidant capability (T-AOC) of the pallium were determined by biochemistry methods. The morphologic changes and Bcl-2 and Bax protein expression in hippocampal CA1 neurons were observed by using hematoxylin- eosin staining and immunohistochemistry staining, respectively. Results: In the SalB group, the MDA content and the NOS activity of the pallium in cerebral ischemia-reperfusion mice significantly decreased and the SOD activity and the T-AOC significantly increased, as compared with the model group (P〈0.05 or P〈0.01). The SalB treatment also rescued neuronal loss (P〈0.01) in the hippocampal CA1 region, strongly promoted Bcl-2 protein expression (P〈0.01) and inhibited Bax protein expression (P〈0.05). Conclusions: SalB increases the level of antioxidant substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SalB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SalB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease. Salvianolic acid B, ischemia-reperfusion, hippocampus, neuron, apoptosis JIANG Yu-feng , LIU Zhi-qin , CUI Wei , ZHANG Wen-tong, GONG Jia-pei , WANG Xi-mei , ZHANG Ying , and YANG Mei-juan (1. Department of Pathology, Beijing University of Chinese Medicine, Beijing 100029, China; 2. Department of Pharmacology, College of Pharmacy, Hebei University, Baoding, Hebei Province 071002, China; 3. Beijing Institute of Heart, Lung and Vessel Diseases, Beijing Anzhen Hospital, Capital University of Medical Sciences, Beijing 100029, China; 4. Department of Province Neurology, Beijing Huimin Hospital, Beijing 100054, China) ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1672-0415 1993-0402 1993-0402 |
DOI: | 10.1007/s11655-014-1791-1 |