title: Phosphorylation of JNK Increases in the Cortex of Rat Subjected to Diabetic Cerebral Ischemia.
abstract: Previous studies have demonstrated that the c-Jun N-terminal kinase (JNK) pathway plays an important role in inducing neuronal apoptosis following cerebral ischemic injury. JNK signaling pathway in activated during cerebral ischemic injury. It participates in ischemia-induced neuronal apoptosis. However, whether JNK signaling is involved in the process of neuronal apoptosis of diabetes-induced cerebral ischemia is largely unknown. This study was undertaken to evaluate the influence of cerebral ischemia-reperfusion injury on phosphorylation of JNK in diabetic rats. Twenty-four adult streptozotocin induced diabetic and 24 adult non-diabetic rats were randomly subjected to 15 min of forebrain ischemia followed by reperfusion for 0, 1, 3, and 6 h. Sixteen sham-operated diabetic and non-diabetic rats were used as controls. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL). Protein expression of phospho-JNK was examined by immunohistochemistry and Western blot. The numbers of TUNEL-positive cells and phospho-JNK protein expression in the cerebral cortices after 1, 3 and 6 h reperfusion was significantly higher in diabetic rats compared to non-diabetic animals subjected to ischemia and reperfusion (p < 0.05). Western blot analysis showed significantly higher phospho-JNK protein expression in the cerebral cortices of the diabetic rats after 1 and 3 h reperfusion than that was presented in non-diabetic animals subjected to ischemia and reperfusion (p < 0.05). These findings suggest that increased phosphorylation of JNK may be associated with diabetes-enhanced ischemic brain damage.
authors.affiliation: Department of Pathology, and Ningxia Key Lab of Craniocerebral Disease, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Ma
authors.affiliation: Department of Neurology, General Hospital, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Shihui
authors.initials: S
authors.lastname: Sun
authors.affiliation: Department of Biology and Genetics, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Jingwen
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Orthopedics, General Hospital, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Zhirong
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Pathology, and Ningxia Key Lab of Craniocerebral Disease, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Fengying
authors.initials: F
authors.lastname: Guo
authors.affiliation: Department of Neurology, General Hospital, Ningxia Medical University, Yinchuan, 750004, China.
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Du
authors.affiliation: Department of Pathology, and Ningxia Key Lab of Craniocerebral Disease, Ningxia Medical University, Yinchuan, 750004, China. zhangjz@nxmu.edu.cn.
authors.forename: Jianzhong
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D048909:Diabetes Complications / Q000378:metabolism* / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000473:pathology; D010766:Phosphorylation; D017207:Rats, Sprague-Dawley
chemical_list: D048031:JNK Mitogen-Activated Protein Kinases
keywords: Cerebral ischemia; Diabetes; Reperfusion; Stroke; c-Jun N-terminal kinase