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dc.contributor.authorÇolak, Ahmet
dc.contributor.authorKaya, Mehmet
dc.contributor.authorKaraoğlan, Alper
dc.contributor.authorSağmanlıgil, Ayhan
dc.contributor.authorAkdemir, Osman
dc.contributor.authorŞahan, Elife
dc.contributor.authorÇelik, Özge
dc.date.accessioned2016-04-28T12:29:08Z
dc.date.available2016-04-28T12:29:08Z
dc.date.issued2009-06
dc.identifier.issn1130-1473
dc.identifier.urihttp://hdl.handle.net/11413/1249
dc.description.abstractBackground. An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. fit this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model. Methods. Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma. Findings. Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 : hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotie cell numbers in groups I and 2 were zero and 4.57 +/- 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 +/- 0.34 cells, a value significantly lower than that in group 2 (P < .05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05). Conclusions. AK 295 inhibited apoptosis via calpain-dependent pathway's and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI.tr_TR
dc.language.isoen_UStr_TR
dc.publisherSoc Espanola Neurocirugia, C/O Dr Poza, Gran Via Salzillo 42, 30005 Murcia, Spaintr_TR
dc.relationNeurocirugiatr_TR
dc.subjectAK 295tr_TR
dc.subjectapoptosistr_TR
dc.subjectcalpain inhibitortr_TR
dc.subjectsecondary damagetr_TR
dc.subjectspinal cord traumatr_TR
dc.subjectactivated neutral proteinasetr_TR
dc.subjectcrystal-structuretr_TR
dc.subjectdown-regulationtr_TR
dc.subjectcalciumtr_TR
dc.subjectbraintr_TR
dc.subjectcalpastatintr_TR
dc.subjectexpressiontr_TR
dc.subjectneuroprotectiontr_TR
dc.subjectdegradationtr_TR
dc.subjectmechanismtr_TR
dc.subjectapoptoztr_TR
dc.subjectikincil hasartr_TR
dc.subjectomurilik travmasıtr_TR
dc.subjectaktive nötr proteinaztr_TR
dc.subjectkristal yapıtr_TR
dc.subjectkalsiyumtr_TR
dc.subjectbeyintr_TR
dc.subjectnörotr_TR
dc.subjectmekanizmatr_TR
dc.subjectbozulmatr_TR
dc.titleCalpain inhibitor AK 295 inhibits calpain-induced apoptosis and improves neurologic function after traumatic spinal cord injury in ratstr_TR
dc.typeArticletr_TR
dc.contributor.authorIDTR113987tr_TR
dc.contributor.authorIDTR110929tr_TR
dc.identifier.wos268685000002
dc.identifier.wos268685000002en
dc.identifier.scopus2-s2.0-70349766092
dc.identifier.scopus2-s2.0-70349766092en


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