| PartⅠ The expression of AQP9 in brain of chronic cerebral ischemia and it,s related mechanismObjectiveTo investigate the expression of AQP9 and MAPK after chronic cerebral ischemia, so as to explore it,s possible role in chronic cerebral ischemia and its corresponding mechanism.MethodsEighty rats were randomly divided into the control group and chronic cerebral ischemia 1, 3 and 6 months groups. Ligation of bilateral common carotid artery(2-vo) was induced to build chronic cerebral ischemia model. The animals were sacrificed after chronic cerebral ischemia. Morris water maze and EPM tests were used to investigate the ability of spatial learning and memory and the anxious emotions; HE staining was used to observe the morp Hological changes after cerebral ischemia; Brain water content(BWC) was measured by the wet-dry weighing ratio method. The content of lactic acid in brain was detected by LD kit. Immunofluorescence was used to investigate the distribution of AQP9 in rat brain. Western blotting was used to test the expression of AQP9, JNK-MAPK, ERK-MAPK and p38-MAPK in brain.ResultsCompared with the control group, the ability of learning and memory of rats decreased significantly in all chronic cerebral ischemia groups. In the EPM test, the total arm entries, open enties/total entries and duration ratios were increased in chronic cerebral ischemia groups. cell arrangement disorder and partial necrosis were observed in chronic cerebral ischemia groups detected by HE staining. Brain water content did not changed significantly in the groups of chronic cerebral ischemia(P<0.05). The content of lactic acid in brain was increased in all groups of chronic cerebral ischemia. The expression of AQP9 was increased in chronic cerebral ischemia groups detected both in immunofluorescence and Western blotting(P<0.05). The ratio of p Hosp Horylated JNK(p-JNK) in JNK, p-p38 in p38 increased, and p-ERK in ERK remained stable after chronic brain inchemia.ConclusionsThe expression of AQP9 was increased after chronic cerebral ischemia, which may participate in transport of lactic acid after chronic brain ischemia. AQP9 could be co-regulated by JNK- MAPK and p38-MAPK pathway.PartⅡ The expression of AQP9 in liver of diabetes mellitus and it,s related mechanismObjectiveTo examine the expression patterns of Aquaporin9(AQP9) and mitogen-activated protein kinase(MAPK) pathway(including JNK, ERK and p38) in Type 1 and Type 2 diabetes mellitus(DM), so as to provide insights into the function and regulatory mechanism of AQP9, and to provide a new idea of the therapy for diabetes.MethodsThe Type 1 DM was established on male adult Sprague-Dawley rats, by intraperitoneal injection once with low dose streptozotocin(STZ). The db/db mice was used as the Type 2 DM. Hematoxylin-eosin staining was used to observe the morp Hological changes in liver. Immunofluorescence was used to investigate the distribution of AQP9 in liver with Type 1 or Type 2 DM. Western blotting was used to test the expression of AQP9, JNK-MAPK, ERK-MAPK and p38-MAPK in liver.ResultsCompared with control group, typical hydropic degeneration, cell arrangemented in disorder and partial necrosis can be observed in liver cells and hepatic sinusoid in both Type 1 and Type 2 DM detected by Hematoxylin-eosin staining. AQP9 expression was observed abundantly towards hepatic sinusoid in both control and diabete group detected by immunofluorescence. Compared with the control group, the expression of AQP9 increased significantly in both Type 1 and Type 2 DM. The ratio of p Hosp Horylated JNK(p-JNK) in JNK increased, p-p38 in p38 decreased, and p-ERK in ERK remained stable in the liver with Type 1 or Type 2 DM.ConclusionsTaken together, AQP9 could be involved in gluconeogenesis and regulated by JNK and p38-MAPK pathway in both Type 1 and Type 2 diabetes mellitus. |
PDF Full Text Request