Phosphorylation of JNK Increases in the Cortex of Rat Subjected to Diabetic Cerebral Ischemia

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• 作者：Yi Ma ; Shihui Sun ; Jingwen Zhang ; Zhirong Chen ; Fengying Guo…
• 关键词：Diabetes ; Cerebral ischemia ; Reperfusion ; c ; Jun N ; terminal kinase ; Stroke
• 刊名：Neurochemical Research
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：41
• 期：4
• 页码：787-794
• 全文大小：1,195 KB
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• 作者单位：Yi Ma (1)
  Shihui Sun (2)
  Jingwen Zhang (3)
  Zhirong Chen (4)
  Fengying Guo (1)
  Yanhui Du (2)
  Jianzhong Zhang (1)
  
  1. Department of Pathology, and Ningxia Key Lab of Craniocerebral Disease, Ningxia Medical University, Yinchuan, 750004, China
  2. Department of Neurology, General Hospital, Ningxia Medical University, Yinchuan, 750004, China
  3. Department of Biology and Genetics, Ningxia Medical University, Yinchuan, 750004, China
  4. Department of Orthopedics, General Hospital, Ningxia Medical University, Yinchuan, 750004, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

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.