ÖZETAmaç: Çalışmamızın amacı tavşan karotis arter anastomoz modelinde gelişen neointimal hiperplazi üzerine bir matriks metalloproteinaz inhibitörü olarak zoledronik asidin (ZA) etkilerini araştırmaktır. Yöntemler: Bu deneysel çalışmada Yeni Zelanda tipi erkek tavşanlar plasebo ve ilaç-tedavi olmak üzere iki gruba ayrılmıştır. Anestezi sonrası, her bir tavşanın sağ karotis arteri 8/0 polipropilen sütür ile uç uca anastomoz edilmiştir. Sol karotis arter ise uygulama olmaksızın kontrol olarak bırakılmıştır. Plasebo grubundaki tavşanlara (n=6) operasyon sonrası 28 gün boyunca PBS (0.5mL/kg/gün/s.k.) uygulanırken ilaç grubundaki tavşanlara (n=6) aynı süre boyunca zoledronik asid (100 μg/kg/gün/s.k.) uygulanmıştır. Sakrifikasyondan sonra anastomozlu ve kontrol arterler izole edilmiştir. Morfometrik ve immünohistokimyasal incelemeler gerçekleştirilmiştir. Morfometrik ve immünohistokimyasal verilerin istatistiksel analizleri sırasıyla çift yönlü ANOVA ve Ki-kare testi ile yapılmıştır. Bulgular: PBS grubunda anastomozlu arterlerde oluşan damar hasarının, kontrol artere kıyasla intimal alanı (kontrol: 22.62±4.26, μm 2 *1000 anastomozlu: 112.51±61.18 μm 2 *1000, p<0.01) ve intima/media indeksini (kontrol: 0.075±0.01, anastomozlu: 0.347±0.29, p<0.05) istatistiksel olarak anlamlı şekilde artırdığı saptanmıştır. Zoledronik asidin, PBS grubuna kıyasla intimal alanı (39.29±18.21 μm 2 *1000, p<0.01) ve intima/media indeksini (0.112±0.07, p<0.05) anlamlı şekilde azaltmıştır. Buna ek olarak, ZA grubundan anastomozlu arterlerde α-düz kas aktin immunpozitivitesi ABSTRACT Objective: The aim of the present study was to investigate the effect of zoledronic acid (ZA), as a matrix metalloproteinase inhibitor, on neointimal hyperplasia in rabbit carotid anastomosis model. Methods: New Zealand male rabbits were divided into two groups as placebo and treatment groups in this experimental study. After anesthesia, the right carotid artery of each rabbit was end-to-end anastomosed with an 8/0 polypropylene suture. Left carotid artery was kept as control without any operation. Placebo group (n=6) received phosphate buffered saline (PBS) (0.5mL/kg/day/s.c.) for 28 days postoperatively, whereas ZA group (n=6) received ZA (100 μg/kg/day/s.c.) for the same period. After sacrification, the anastomosed and control arteries were isolated. Morphometric and immunohistochemical examinations were performed. Statistical analyses of morphometric and immunohistochemical data were performed using two-way ANOVA and Chi-square test respectively. Results: In PBS group, vascular injury in the anastomosed artery significantly increased the intimal area (anastomosed: 112.51±61.18 μm 2 *1000 vs. control: 22.62±4.26μm 2 *1000, p<0.01) and intima/media index (anastomosed: 0.347±0.29 vs. control: 0.075±0.01, p<0.05) compared to control artery. ZA significantly reduced the intimal area (39.29±18.21 μm 2 *1000 , p<0.01) and intima/media index (0.112±0.07, p<0.05) compared to PBS group. Additionally, α-smooth muscle actin immunopositivity was found significantly decrease...
Peripheral nerve injury primarily occurs due to trauma as well as factors such as tumors, inflammatory diseases, congenital deformities, infections, and surgical interventions. The surgical procedure to be performed as treatment depends on the etiology, type of injury, and the anatomic region. The goal of treatment is to minimize loss of function due to motor and sensory nerve loss at the distal part of the injury. Regardless of the cause of the injury, the abnormal nerve regeneration due to incomplete nerve regeneration, optimal treatment of peripheral nerve injuries should provide adequate coaptation of proximal and distal sides without tension, preserving the neurotrophic factors within the repair line. The gold standard for the treatment of nerve defects is the autograft; however, due to denervation of the donor site, scarring, and neuroma formation, many studies have aimed to develop simpler methods, better functional results, and less morbidity. In this study, a defect 1 cm in length was created on the sciatic nerve of rats. The rats were treated with the following procedures: group 1, autograft; group 2, allogeneic aorta graft; group 3, diced cartilage graft in allogeneic aorta graft; and group 4, tubularized cartilage graft in allogeneic aorta graft. Group 5 was the control group. The effects of cartilage tissue in nerve regeneration were evaluated by functional and histomorphological methods.Group 1, for which the repair was performed with an autograft, was evaluated to be the most similar to the control group. There was not a statistically significant difference in myelination and Schwann cell rates between group 2, in which an allogeneic aorta graft was used, and group 3, in which diced cartilage in an allogeneic aorta graft was used. In group 4, myelination and Schwann cell formation were observed; however, they were scattered and irregular, likely due to increased fibrosis.In all of the groups, nerve regeneration at various rates was observed both functionally and histomorphologically. This study demonstrates that cartilage tissue has promoting effects in nerve regeneration.
Introduction: The aim of this study was to investigate how melatonin administration for 3 days or 7 days following cerebral ischemia injury (CI/R) would affect autophagy, and therefore, survival in neurons of the penumbra region. Moreover, it was also aimed to determine how this melatonin treatment would affect the neurological deficit score and rotarod and adhesive removal test durations. Methods: Focal CI (90 min) was achieved in a total of 105 rats utilizing a middle cerebral artery occlusion model. After the start of reperfusion, the groups were treated with melatonin (10 mg/kg/day) for 3-days or 7-days. On all groups, neurological deficit scoring, rotarod and adhesive removal test were executed during reperfusion. Infarct areas were determined by TTC (2,3,5-triphenyltetrazolium chloride) staining at the end of the 3rd and 7th days of reperfusion. Beclin-1, LC3, p62 and caspase-3 protein levels were assessed using Western blot and immunofluorescence methods in the brain tissues. Moreover, penumbra areas were evaluated by transmission electron microscopy (TEM). Results: Following CI, it was observed that melatonin treatment improved the rotarod and adhesive removal test durations from day 5 and reduced the infarct area after CI. It also induced autophagic proteins Beclin-1, LC3 and p62 and suppressed the apoptotic protein cleaved caspase-3. According to TEM findings, melatonin treatment partially reduced the damage in neurons after CI. Conclusion: Melatonin treatment following CI reduced the infarct area and induced the autophagic proteins Beclin-1, LC3 and p62 via inhibiting the apoptotic caspase-3 protein. The functional reflection of melatonin treatment on neurological tests scores was became significant from the 5th day onward.
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