Protective Effects of Shikonin on Brain Injury Induced by Carbon Ion Beam Irradiation in Mice

Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed protective effect on cerebral ischemic injury. Here we investigated the effects of shikonin on carbon ion beam induced radiation brain injury in mice. Pretreatment with shikonin significantly increased the SOD and CAT activities and the ratio of GSH/GSSG in mouse brain tissues compared with irradiated group （P〈0.01）, while obviously reduced the MDA and PCO contents and the RO$ levels derived from of the brain mitochondria.

New Stroke-healing Gel Helped Regrow Neurons and Blood Vessels in Mice with Stroke-damaged Brains, Hinting at What May Someday Be a New Therapy for Stroke in People

In a first-of-its-kind finding,a new stroke-healing gel helped regrow neurons and blood vessels in mice with stroke-damaged brains.The results suggest that such an approach may someday be a new therapy for stroke in people.The study tested this in laboratory mice to determine if it would repair the brain in a model

Neuroprotective Effects of Electroacupuncture Preventive Treatment in Senescence-Accelerated Mouse Prone 8 Mice

Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.

Temporary and permanent focal cerebral ischemia in the mouse: assessment of cerebral blood flow, brain damage and blood-brain barrier permeability

Objective To establish a mouse model of middle cerebral artery occlusion, which mimics focal ischemia in humans and to demonstrate the advantages and disadvantages of the model Methods CD 1 mice (n=126) had permanent middle cerebral artery occlusion for 24?h, or temporary occlusion for either one hour followed by 23?h of reperfusion or 2?h of occlusion with 22?h of reperfusion The middle cerebral artery was occluded by insertion of a suture through the internal carotid artery Reperfusion was established by suture withdrawal The degree of occlusion and the extent of reperfusion were determined using laser Doppler Infarct volume was measured with 2, 3, 5 triphenyl tetrazolium chloride staining, and the blood brain barrier disruption was demonstrated using albumin immunohistochemistry Results Blood flow decreased to 14%-19% of baseline in both the permanent and temporary occlusion groups and was restored to 51%-75% of baseline after reperfusion The infarct volume was smaller in the 1?h/23?h temporary occlusion group ( P <0 05) than in either the 24?h permanent occlusion group or the 2?h/22?h temporary occlusion group Blood brain barrier disruption was also smaller in the 1?h/23?h temporary occlusion group than in either the 24?h permanent occlusion or the 2?h/22?h temporary occlusion group ( P <0 05) Conclusion Permanent or temporary middle cerebral artery occlusion causes reproducible brain injury in the mouse Blood brain barrier disruption and infarct volume remain important markers of focal cerebral ischemia