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

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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.

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Acknowledgments

Yi Ma was supported by National Natural Science Foundation of China (No. 81360196) and Natural Science Foundation of Ningxia Province (No. NZ13066). The authors appreciate Dr. P. Andy Li at North Carolina Central University for critical discussion and proofreading.

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Correspondence to Jianzhong Zhang.

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This article does not contain any studies with human participants performed by any of the authors.

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The authors declare that they have no conflict of interest to this study.

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All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.

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Yi Ma and Shihui Sun have contributed equally to this study and share first authorship.

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Ma, Y., Sun, S., Zhang, J. et al. Phosphorylation of JNK Increases in the Cortex of Rat Subjected to Diabetic Cerebral Ischemia. Neurochem Res 41, 787–794 (2016). https://doi.org/10.1007/s11064-015-1753-4

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  • DOI: https://doi.org/10.1007/s11064-015-1753-4

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