The Expression Changes Of AQP4 And AQP9 In Brain Tissue After Chronic Cerebral Ischemia And Their Mechanism Of Action

Objective: To investigate the expression of aquaporin 4(AQP4)and explore its possible role in chronic cerebral ischemia.Methods: 40 SD rats were selected as experimental objects.According to the random number table method,those rats were randomly subdivided into the control group(group N,n=10)and the experiment group;based on cerebral ischemia time,the experiment group was sub divided into 2 weeks group(group 2W,n=10),1 month group(group 1M,n=10)and 2 months group(group 2M,n=10).A rat model of chronic cerebral ischemia was induced by bilateral common carotid artery ligation.The brain water content was measured by dry and wet weighting ration method,and the general histology of brain tissue was evaluated and analyzed by hematoxylin eosin staining.The distribution of AQP4 protein was detected by immunofluorescence,and the relative expression of AQP4 protein was detected by Western blotting.Results: There was no significant difference for brain water content between the control group and experimental group(P>0.05).The results of hematoxylin eosin staining showed that compared with the control group,the local nuclei of brain tissue in the experiment group exhibited partial pyknosis or disappeared,and some cells were apoptotic and necrotic.The results of western blotting and immunofluorescence showed that the expression level of AQP4 in the experiment group was significantly increased,compared with the control group.As the ischemia time prolonged,AQP4 expression was further up-regulated and colocalized with IBa1Conclusions: Chronic cerebral ischemia could result in neuron apoptosis,microglia activation and proliferation and up-regulation of AQP4,suggesting that AQP4 may be involved in the inflammatory process after ischemia.Objective: To investigate the expression of AQP9,glycerol and MAPK signal pathway in brain after chronic cerebral ischemia,so as to explore the possible role of AQP9 in chronic cerebral ischemia and its regulating mechanism.Methods: 60 SD rats were selected as experimental objects.According to the random number table method,these rats were randomly divided into the control group(group N,n=15)and the experiment group;based on cerebral ischemia time,the experiment group was sub divided into 2 weeks group(group 2W,n=15),1 month group(group 1M,n=15)and 2 months group(group 2M,n=15).Ligation of bilateral common carotid artery(2-vo)was induced to build chronic cerebral ischemia model.Morris water maze was used to investigate the ability of spatial learning and memory.The content of glycerol in brain was detected by enzyme assay kit.Immunofluorescence was used to investigate the distribution of AQP9 in rat brain.Western blotting was used to test the expression of AQP9,CREB and MAPK in brain.Results: Compared with the control group,the ability of learning and memory was decreased significantly in all chronic cerebral ischemia groups.The content of glycerol in brain was increased in all groups of chronic cerebral ischemia.The expression of AQP9 was increased in chronic cerebral ischemia groups detected by Western blotting(P<0.05).The ratio of phosphorylated CREB in CREB,phosphorylated JNK(p-JNK)in JNK,phosphorylated p38(p-p38)in p38 and phosphorylated ERK(p-ERK)in ERK was increased after chronic brain ischemia.Conclusions: The expression of AQP9 was increased after chronic cerebral ischemia,which may participate in glycerol transportation after chronic brain ischemia.AQP9 could be co-regulated by JNK-MAPK,p38-MAPK and p-ERK in ERK pathway.