Zhi He1, Zhihong Pan, Wenhong Lu. 1. Medical School, China Three Gorges University, Yichang 443002, China. hezhi2003@126.com
Abstract
OBJECTIVE: To investigate the underlying neuroprotective mechanisms of Tanshinone II A (TSA) on rat cerebral ischemia in vivo. METHOD: Study of TSA on rat cerebral ischemia in vivo: Male SD rats were divided into four groups (sham-operated, ischemic and treated group (lower dose and higher dose). Chronic cerebral ischemmia after permanent bilateral carotid artery ligation was introduced as an in vivo ischemic model. After ischemia impairment, TSA (2, 4 mg x kg(-1) x d(-1)) was administrated by ip for 30 days in treated group. We used Morris water maze to investigate the learning and memory. Levels of malondialdehyde (MDA), activity of superoxide dismetase (SOD) and glutathione peroxidase (GPX) in brain tissue were detected by spectrophotometer. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the contents of glutamate and gamma-aminobutyric acid (GABA) in cortex and hippocampus. RESULTS: TSA can improve learning and memory deficits in vascular dementia. An elevation of SOD and GPX activity and decrease of MDA level were shown in TSA treated group after brain ischemia. Decreased glutamate and gamma-aminobutyric acid induced by chronic brain ischemia were markedly inhibited by TSA pretreatment. CONCLUSION: The neuroprotective effect of TSA are partly due to its functions as follow: anti-free radical injury; regulating the content of glutamate and gamma-aminobutyric acid.
OBJECTIVE: To investigate the underlying neuroprotective mechanisms of Tanshinone II A (TSA) on ratcerebral ischemia in vivo. METHOD: Study of TSA on ratcerebral ischemia in vivo: Male SD rats were divided into four groups (sham-operated, ischemic and treated group (lower dose and higher dose). Chronic cerebral ischemmia after permanent bilateral carotid artery ligation was introduced as an in vivo ischemic model. After ischemia impairment, TSA (2, 4 mg x kg(-1) x d(-1)) was administrated by ip for 30 days in treated group. We used Morris water maze to investigate the learning and memory. Levels of malondialdehyde (MDA), activity of superoxide dismetase (SOD) and glutathione peroxidase (GPX) in brain tissue were detected by spectrophotometer. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the contents of glutamate and gamma-aminobutyric acid (GABA) in cortex and hippocampus. RESULTS:TSA can improve learning and memory deficits in vascular dementia. An elevation of SOD and GPX activity and decrease of MDA level were shown in TSA treated group after brain ischemia. Decreased glutamate and gamma-aminobutyric acid induced by chronic brain ischemia were markedly inhibited by TSA pretreatment. CONCLUSION: The neuroprotective effect of TSA are partly due to its functions as follow: anti-free radical injury; regulating the content of glutamate and gamma-aminobutyric acid.
Authors: Xinhua Zhou; Guozhen Cui; Hisa Hui Ling Tseng; Simon Ming-Yuen Lee; George Pak Heng Leung; Shun Wan Chan; Yiu Wa Kwan; Maggie Pui Man Hoi Journal: Evid Based Complement Alternat Med Date: 2016-11-23 Impact factor: 2.629