The protective mechanisms of hyperbaric oxygen therapy in a middle cerebral artery occlusion rat model

• Main Authors: Huang Ling Yi, 黃鈴詒
• Other Authors: 牛柯琪
• Format: Others
• Language: zh-TW
• Published: 101
• Online Access: http://ndltd.ncl.edu.tw/handle/41849433382785613656

碩士 === 南台科技大學 === 生物科技系 === 100 === According to the World Health Organization and the cause of death in Taiwan the sequelae of cerebral vascular disease are highest in the second in which the incidence of ischemic stroke account for about 70 percent of all types of stroke. There are many barriers in the present treatment, such as cerebral anoxia and edema of the vicious circle resulting in rapid increase in intracranial pressure, formation of new lesions or bleeding during the rehabilitation process of stroke, difficulty to grasp the changing condition in stroke, etc. Hyperbaric oxygen therapy has been widely applied to many critical disorders such as crushing injury, burns, cerebral ischemic diseases, carbon monoxide poisoning, and necrotizing fasciitis through the mechanism of increasing tissue oxygen tension, improving the local circulation and resuming the normal metabolism. Recently, hyperbaric oxygen therapy （HBO）has been also successfully applied to ischemic stroke, traumatic head injury, cerebral hemorrhage, acute and chronic cerebral ischemia, etc. To further investigate the effect of HBO on middle cerebral artery occlusion (MCAo) possible mechanisms, we design a series of animal studies. In the present study, we examined alterations in glial and neuronal cell responses to the reported neuroprotection of hyperbaric oxygen against cerebral ischemia. Focal cerebral ischemia (for 90 minutes) was induced by MCAo with a 4-0 monofilament nylon suture line, coated with poly-L-lysine, which was introduced from the common carotid artery (CCA) into the internal carotid artery until a mild resistance were felt (18 to 19 mm), thereby occluding the origin of the MCA. Rats were randomly divided into seven groups: sham operation group, middle cerebral artery occlusion group (3ady, 3D), middle cerebral artery occlusion (MCAo) with once HBO treatment group (3D1T), MCAo with four times HBO treatment group (3D4T), MCAo group (7ady, 7D), MCAo with once HBO treatment group (7D1T), MCAo with four times HBO treatment group (7D4T). Adult Sprague-Dawley rats were given HBO treatment immediately after 90 mins occlusion of the middle cerebral artery. Rats were killed at 3 days or 7days to harvest tissues for lipid peroxidation, TTC stain, Brain swelling, maximum grip angle, TUNEL, and immunofluorescent studies of GFAP, NeuN and BrdU to evaluate the neurogenesis. Our results revealed that, after the MCAo, the infarct volume, motor dysfunction and brain swelling were all significantly increased. Similarly, the number of GFAP positive cell was significantly elevated in the cortex of rat brain after at 3days and 7days after reperfusion, and result in neuronal apoptosis, gliosis and locomotor dysfuction. HBO treatment significantly enhanced survival of neuron at 3 days and 7 days after reperfusion of the MCAo, and the preservation of these glial cells in the ischemic brain corresponded with a markedly reduced area of infarction as well as increased neuronal survival. These results suggest that HBO may cause attenuation of cerebral infarction as well as motor deficits by enhancing neuronal survival.