Neural Regeneration Research ›› 2017, Vol. 12 ›› Issue (1): 96-102.doi: 10.4103/1673-5374.198992

Previous Articles     Next Articles

Inhibition of cerebral ischemia/reperfusion injuryinduced apoptosis: nicotiflorin and JAK2/STAT3 pathway

Guang-qiang Hu1, Xi Du2, Yong-jie Li3, Xiao-qing Gao4, Bi-qiong Chen2, Lu Yu2   

  1. 1 Department of Anatomy, Southwest Medical University, Luzhou, Sichuan Province, China; 
    2 Department of Chemistry, Southwest Medical University, Luzhou, Sichuan Province, China; 
    3 Drug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan Province, China; 
    4 Department of Anatomy and Neurobiology, Southwest Medical University, Luzhou, Sichuan Province, China
  • Received:2016-10-22 Online:2017-01-15 Published:2017-01-15
  • Contact: Guang-qiang Hu or Lu Yu, hgq863@sina.com or yulu863@sina.com.
  • Supported by:

    This study was mainly supported by the National Science Foundation of Education Department of Sichuan Province of China, No. 14ZB0152; the Joint Research Program of Luzhou and Luzhou Medical College, No. 14JC0120.

PDF

836

Abstract:

Nicotiflorin is a flavonoid extracted from Carthamus tinctorius. Previous studies have shown its cerebral protective effect, but the mechanism is undefined. In this study, we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway. The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion. Nicotiflorin (10 mg/kg) was administered by tail vein injection. Neuronal apoptosis was examined by hematoxylin-eosin staining andterminal deoxynucleotidyl transferase dUTP nick end labeling assay. Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining. Additionally, p-JAK2, p-STAT3, Bcl-2, Bax, and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay. Our results show that nicotiflorin alters the shape and structure of injured neurons, decreases the number of apoptotic neurons, down-regulates expression of p-JAK2, p-STAT3, caspase-3, and Bax, decreases the immune response of Bax, and up-regulates expression of Bcl-2 protein and the immune response. These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.

Key words: nerve regeneration, brain injury, nicotiflorin, ischemic stroke, cerebral ischemia/reperfusion injury, treatment, cell apoptosis, terminal deoxynucleotidyl transferase dUTP nick end labeling, JAK2/STAT3 pathway, Bcl-2, Bax, caspase-3, neural regeneration