Batroxobin protects against spinal cord injury in rats by promoting the expression of vascular endothelial growth factor to reduce apoptosis
Identifieur interne : 007565 ( Ncbi/Checkpoint ); précédent : 007564; suivant : 007566Batroxobin protects against spinal cord injury in rats by promoting the expression of vascular endothelial growth factor to reduce apoptosis
Auteurs : Hui Yu [République populaire de Chine] ; Bin Lin [République populaire de Chine] ; Yongzhi He [République populaire de Chine] ; Wenbin Zhang [République populaire de Chine] ; Yang Xu [République populaire de Chine]Source :
- Experimental and Therapeutic Medicine [ 1792-0981 ] ; 2015.
Abstract
The host response to spinal cord injury (SCI) can lead to an ischemic environment that can induce cell death. Therapeutic interventions using neurotrophic factors have focused on the prevention of such reactions in order to reduce this cell death. Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. We hypothesized in this study that batroxobin would exhibit protective effects following SCI by promoting the expression of VEGF to reduce the levels of apoptosis in a rat model of SCI. Ninety adult female Sprague Dawley rats were divided randomly into sham injury (group I), SCI (group II) and batroxobin treatment (group III) groups. The Basso-Bettie-Bresnahan (BBB) scores, number of apoptotic cells and expression of VEGF were assessed at 1, 3, 5, 7, 14 and 28 days post-injury. The BBB scores were significantly improved in group III compared with those in group II between days 5 and 28 post-injury (P<0.05). At each time-point subsequent to the injury, the number of apoptotic cells in group III was reduced compared with that in group II. Compared with group II, treatment with batroxobin significantly increased the expression of VEGF from day 3 until 2 weeks post-SCI (P<0.05), while no significant difference was observed at day 28. These data suggest that batroxobin has multiple beneficial effects on SCI, indicating a potential clinical application.
Url:
DOI: 10.3892/etm.2015.2368
PubMed: 26136870
PubMed Central: 4471772
Affiliations:
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China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000</wicri:regionArea><wicri:noRegion>Fujian 363000</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Bin" sort="Lin, Bin" uniqKey="Lin B" first="Bin" last="Lin">Bin Lin</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-2368">Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000</wicri:regionArea><wicri:noRegion>Fujian 363000</wicri:noRegion></affiliation></author><author><name sortKey="He, Yongzhi" sort="He, Yongzhi" uniqKey="He Y" first="Yongzhi" last="He">Yongzhi He</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-2368">Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000</wicri:regionArea><wicri:noRegion>Fujian 363000</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Wenbin" sort="Zhang, Wenbin" uniqKey="Zhang W" first="Wenbin" last="Zhang">Wenbin Zhang</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-2368">Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000</wicri:regionArea><wicri:noRegion>Fujian 363000</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Yang" sort="Xu, Yang" uniqKey="Xu Y" first="Yang" last="Xu">Yang Xu</name><affiliation wicri:level="1"><nlm:aff id="af1-etm-0-0-2368">Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000, P.R. China</nlm:aff><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Orthopedics, The 175th Hospital of the PLA, Southeast Hospital of Xiamen University, Zhangzhou, Fujian 363000</wicri:regionArea><wicri:noRegion>Fujian 363000</wicri:noRegion></affiliation></author></analytic><series><title level="j">Experimental and Therapeutic Medicine</title><idno type="ISSN">1792-0981</idno><idno type="eISSN">1792-1015</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The host response to spinal cord injury (SCI) can lead to an ischemic environment that can induce cell death. Therapeutic interventions using neurotrophic factors have focused on the prevention of such reactions in order to reduce this cell death. Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. We hypothesized in this study that batroxobin would exhibit protective effects following SCI by promoting the expression of VEGF to reduce the levels of apoptosis in a rat model of SCI. Ninety adult female Sprague Dawley rats were divided randomly into sham injury (group I), SCI (group II) and batroxobin treatment (group III) groups. The Basso-Bettie-Bresnahan (BBB) scores, number of apoptotic cells and expression of VEGF were assessed at 1, 3, 5, 7, 14 and 28 days post-injury. The BBB scores were significantly improved in group III compared with those in group II between days 5 and 28 post-injury (P<0.05). At each time-point subsequent to the injury, the number of apoptotic cells in group III was reduced compared with that in group II. Compared with group II, treatment with batroxobin significantly increased the expression of VEGF from day 3 until 2 weeks post-SCI (P<0.05), while no significant difference was observed at day 28. These data suggest that batroxobin has multiple beneficial effects on SCI, indicating a potential clinical application.</p></div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yu, Hui" sort="Yu, Hui" uniqKey="Yu H" first="Hui" last="Yu">Hui Yu</name></noRegion><name sortKey="He, Yongzhi" sort="He, Yongzhi" uniqKey="He Y" first="Yongzhi" last="He">Yongzhi He</name><name sortKey="Lin, Bin" sort="Lin, Bin" uniqKey="Lin B" first="Bin" last="Lin">Bin Lin</name><name sortKey="Xu, Yang" sort="Xu, Yang" uniqKey="Xu Y" first="Yang" last="Xu">Yang Xu</name><name sortKey="Zhang, Wenbin" sort="Zhang, Wenbin" uniqKey="Zhang W" first="Wenbin" last="Zhang">Wenbin Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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