Literature DB >> 24228092

Influences of HIF-lα on Bax/Bcl-2 and VEGF expressions in rats with spinal cord injury.

Mao-Hua Chen1, Qing-Xian Ren, Wen-Fa Yang, Xiang-Lin Chen, Chuan Lu, Jun Sun.   

Abstract

Hypoxia-inducible factor 1-alpha (HIF-1α) is a subunit of HIF-l and thought to be able to protect hypoxic cells from apoptosis or necrosis under ischemic and anoxic conditions. This study aimed to investigated whether recombinant adenovirus vector over-expressing HIF-lα could affect apoptosis-related proteins (Bcl-2 and Bax) and vascular endothelial growth factor (VEGF) in a rat spinal cord injury (SCI) model. A total of 60 male SD rats were divided into 4 groups: Sham, Control, Ad-Blank and Ad-HIF-1α groups. 1, 3, 7, 14, 28 days after surgery, the behavioral recovery was evaluated with BBB scales. Then, rats were sacrificed and the spinal cord was collected for detection of Bcl-2, Bax and VEGF expressions by immunohistochemistry. Results showed the Bcl-2, Bax, VEGF and HIF-lα expressions increased in animals with SCI, but the increase in Bcl-2, VEGF and HIF-lα expressions were higher in Ad-HIF-1α group when compared with other groups, but Bax expression decreased significantly. In addition, administration of Ad-HIF-1α significantly reduced apoptotic cells and promoted the recovery of neurological function. In conclusion, administration of Ad-HIF-1α after SCI could ameliorate neuronal apoptosis and promote angiogenesis in rats. Our study provides a basis for further exploration of the relationship between HIF1α and SCI.

Entities:  

Keywords:  HIF-1α; apoptosis; spinal cord injury; vascular endothelial growth factor

Mesh:

Substances:

Year:  2013        PMID: 24228092      PMCID: PMC3816799     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


  28 in total

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  14 in total

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Journal:  Int J Clin Exp Pathol       Date:  2015-04-01

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Authors:  Ningning Liu; Lei Chen; Na Cai
Journal:  Int J Clin Exp Pathol       Date:  2015-05-01

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8.  Pretreatment with AQP4 and NKCC1 Inhibitors Concurrently Attenuated Spinal Cord Edema and Tissue Damage after Spinal Cord Injury in Rats.

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