Objective To observe the effect of early mild hypothermia on the opening of tight junction of cerebral endothelial cells following traumatic brain injury in order to illustrate possible mechanism of low permeability of blood brain barrier (BBB) treated by mild hypothermia. Methods A total of 90 Wistar rats were randomly divided into normothermia control group (n=10),normothermia injury group (n=40) and mild hypothermia group (n=40). The opening state and its extent of tight junction were observed using lanthanum trace labeling with electron microscope. At the same time,water content of cerebral tissue at different phases in normothermia injury group and mild hypothermia group was measured by means of dry-wet weight and analyzed statistically. Results The tight junction was under preliminary opening three hours after trauma and reached the maximum opening within 24-48 hours after trauma,lasting for 72 hours in the normothermia injury group. However,slight opening appeared only in the mild hypothermia group. Water content of cerebral tissue in the mild hypothermia group lessened obviously in contrast to that in the normothermia injury group,with significant difference 3,24 and 72 hours after trauma ( P

Objective We investigate lipid peroxidation of compressed myeloid tissue at early stage after decompression of chronic compressive spinal cord injury.Method SOD and MDA of compressed myeloid tissue are measured respectively before compression,before decompression and 3h after decompression.Result Increased MDA while decreased SOD of compressed myeloid tissue at 3h after decompression than before decompression.Conclusion The increased lipid peroxidation of compressed myeloid tissue at early stage after decompression of chronic compressive spinal cord injury.It is possible that it was resulted from ischemical reperfusion injury.

Objective To investigate the protective effects of piceatannol on retinal ganglion cells (RGCs) in rats with glaucoma.Methods Forty rats were randomly divided into 4 groups:control group,model group,low dose piceatannol treatment group and high dose piceatannol treatment group.Photocoagulation method was used to establish the experimental glaucoma model in rats,and then rats were given 100 mg· kg-1 or 200 mg · kg-1 of piceatannol by gavage.The intraocular pressure was measured before and after the model was established.Rat retinal ganglion cells were labeled and counted using FG staining.Retinal tissue pathological morphology was observed by HE staining.The protein expression of p-JNK,p-c-Jun,p-ERK,p-p38 MAPK and TNF-α were measured by western blot.Results Compared with control group,the intraocular pressure,the protein expressions of p-JNK,p-c-Jun p-ERK,p-p38 MAPK and TNF-α were significantly increased in model group (all P ＜ 0.05).However,the number of RGCs were lower in model group(P ＜0.05).Furthermore,there were cavitation and edema changes in retinal tissue of model group.Compared with model group,piceatannol treatment markediy increased the number of RGCs(P =0.003,0.002),improved the pathological morphology of retinal tissue,and reduced the protein expressions of p-JNK,p-c-Jun p-ERK,p-p38 MAPK and TNF-α (all P ＜ 0.05),especially for the high concentration.Conclusion Piceatannol can protect against RGCs injury in glaucoma rats,and the mechanism may be associated with inhibition of MARK signaling pathway.