Birgul Yigitcan

Comparison of Nerve, Vessel, and Cartilage Grafts in Promoting Peripheral Nerve Regeneration

AbstractPeripheral 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.

Calculation of melatonin and resveratrol effects on steatosis hepatis using soft computing methods

In this work, beneficial effects of melatonin and resveratrol drugs on liver damage in rats, induced by application of acute and chronic carbon tetrachloride (CCl4) have been examined. The study consists of three main stages: (1) DATA ACQUISITION: light microscopic images were obtained from 60 rats separated into 10 groups after the preparation of liver tissue samples for histological examination. Rats in first five experimental groups for the four-day and the other five groups for twenty-day were examined. (2) Data processing: by the help of histograms of oriented gradient (HOG) method, obtaining low-dimensional image features (color, shape and texture) and classifying five different group characteristics by using these features with artificial neural networks (ANNs), and support vector machines (SVMs) have been provided. (3) Calculation of drug effectiveness: firstly to determine the differences between group characteristics of rats, a pilot group has been selected (diseased group-CCl4), and the responses of ANN and SVM trained by HOG features have been calculated. As a result of ANN, it has been seen that melatonin and resveratrol drugs have %65.62-%75.12 positive effects at the end of the fourth day, %84.12-%98.89 positive effects on healing steatosis hepatis at the end of the twentieth day respectively and as a result of SVM, it has been seen that melatonin and resveratrol drugs have %62.5-%68.75 positive effects at the end of the fourth day, %45.12-%60.89 positive effects on healing steatosis hepatis at the end of the twentieth day respectively.

Hepatoprotective effects of crocin on biochemical and histopathological alterations following acrylamide-induced liver injury in Wistar rats

The objective of the present study is the treatment of oxidative damage caused by acrylamide induced oxidative stress in rats with the administration of a strong antioxidant, namely crocin. High acrylamide (AA) levels have genotoxic, carcinogenic and neurotoxic effects on living organisms. In the present study, 40 Wistar rats were randomly divided into four equal groups. These groups were control, acrylamide (25mg/kg), crocin (50mg/kg), acrylamide+crocin (25mg/kg acrylamide and 50mg/kg crocin) groups. At the end of the application, biochemical and histological variations were examined in liver and blood samples. It was observed that acrylamide administration significantly decreased liver GSH and TAS levels when compared to the control group. On the contrary, it was also observed that AST, ALT, ALP, SOD and CAT activities and TOS and MDA levels increased as a result of acrylamide administration. Histopathological examinations demonstrated inflammatory cell infiltration, hepatocellular necrosis and hemorrhage areas in AA group liver sections. Furthermore, intracytoplasmic vacuolization was detected in hepatocytes. After crocin treatment, it was observed that GSH and TAS levels increased while AST, ALT, ALP, SOD and CAT activities and TOS and MDA levels decreased. Significant decreases were observed in inflammatory cell infiltration and vascular congestion in liver sections and intracytoplasmic vacuolization in hepatocytes after the crocin treatment, while no hepatocellular necrosis and hemorrhages were observed. In the present study, it was demonstrated that crocin treatment removed acrylamide induced liver damage due to the strong antioxidant properties of crocin.

Protective Effects of Alpha-Lipoic Acid on Methotrexate-Induced Oxidative Lung Injury in Rats

ABSTRACT Objective: Oxidative stress is one of the major causes of methotrexate induced lung injury (MILI). Alpha-lipoic acid (ALA), which occurs naturally in human food, has antioxidative and anti-inflammatory activities. The aim of this study was to research the potential protective role of ALA on MILI in rats. Methods: Twenty one rats were randomly subdivided into three groups: control (group I), methotrexate (MTX) treated (group II), and MTX+ALA treated (group III). Lung injury was performed with a single dose of MTX (20 mg/kg) to groups 2 and 3. On the sixth day, animals in all groups were sacrificed by decapitation and lung tissue and blood samples were removed for histological examination and also measurement the levels of interleukin-1-beta (IL-1β), malondialdehyde (MDA), glutathione (GSH), tumour necrosis factor-alpha (TNF-α), myeloperoxidase (MPO), and sodium potassium-adenosine triphosphatase (Na+/K+ATPase). Results: In MTX group tissue GSH, Na+/K+ATPase activities were lower, tissue MDA, MPO and plasma IL-1?, TNF-? were significantly higher than the other groups. Histopathological examination showed that lung injury was less severe in group 2 according to group 3. Conclusions: Oxidative damage of MTX in rat lung is partially reduced when combined with ALA.

Acrylamide applied during pregnancy causes the neurotoxic effect by lowering BDNF levels in the fetal brain

OBJECTIVES The aim of this study is to elucidate the possible mechanism of neurotoxic effect of acrylamide (AA) applied during pregnancy on fetal brain development and to show the effect of N-acetylcysteine (NAC) on AA toxicity. MATERIALS AND METHODS Four groups were formed with 9 pregnant rats each as control (C), acrylamide (AA), N-acetylcysteine (NAC), acrylamide plus N-acetylcysteine (AA plus NAC) groups. Caesarian section was implemented on the 20th day of pregnancy. Malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and Brain-derived neurotrophic factor (BDNF) levels were analyzed and histopathologic examinations were performed in brain tissues of the fetuses. RESULTS Our data indicated that AA caused necrotic death and hemorrhagic damages in fetal brain tissue with decreasing BNDF levels and increasing oxidative stress. N-acetylcysteine prevented the toxic effects of its on fetal brain (p < 0.05). CONCLUSION Our study indicated that acrylamide has toxic effects in the fetal brain and N-acetylcysteine prevents its toxic effect.

Melatonin preserves ovarian tissues of rats exposed to chronic TCDD: An electron microscopic approach to effects of TCDD on ovarian cells

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a toxic agent and has disruptive effects on reproductive tissues in females. TCDD disrupts the hormonal regulation of the body and decreases the production of melatonin. In this study, we investigated the protective effects of melatonin supplements against the toxic effects of TCDD on ovaries of female rats. TCDD caused a significant decrease in the average number of corpora lutea and follicles per tissue section (2.1 ± 0.7; 2.3 ± 0.8, respectively), whereas these numbers were maintained in the melatonin supplemented group (5.0 ± 0.8; 5.1 ± 0.8, respectively) and were similar to the control group (5.3 ± 1.0; 5.9 ± 0.9, respectively). Electron microscopic analysis showed that the disruption of ultrastructure components such as cell membrane and organelles due to TCDD exposure was inhibited by melatonin supplements. This study suggested that melatonin has a protective and a possible ameliorative effect over histopathological damage of rat ovaries exposed to TCDD.

The effects of acrylamide and vitamin E on kidneys in pregnancy: an experimental study

Abstract Objectives: The objective of this study is to investigate possible damages to kidney tissues of pregnant rats and their fetuses exposed to acrylamide during pregnancy and possible protective effects of vitamin E against these damages. Material and methods: Rats were randomly assigned to five groups of control, corn oil, vitamin E, acrylamide, vitamin E + acrylamide, six pregnant rats in each. Mother and fetal kidney tissues were examined for malondialdehyde (MDA), reductase glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS), total oxidant status (TOS), urea, creatine, trace elements such as Zn and Cu in the serum and histopathological analyses were conducted. Results: It was determined that acrylamide, administered during pregnancy, statistically significantly increased MDA and TOS levels, maternal serum urea, creatinine, and Zn levels, while it decreased GSH, TAS, SOD, and CAT levels (p ≤ .05) when compared with all other groups in the kidney tissues of pregnant rats and their fetuses and caused tubular degeneration, hemorrhage, narrowing, and closure in Bowman’s space, and, in the E vitamin group, it statistically significantly increased GSH, TAS, SOD, CAT, urea, creatinine, and Zn levels when compared with other groups and lowered TOS and MDA levels to those of the control group (p < .05) and there were no differences between the groups histologically. Conclusion: It was observed that acrylamide administered during pregnancy caused oxidative stress in kidney tissues of mother rats and their fetuses, resulting in tissue damage, and vitamin E application, which is considered to be a powerful antioxidant, inhibited oxidative stress.

Effects of Melatonin and Dexamethasone on Facial Nerve Neurorrhaphy

OBJECTIVES To investigate the effects of topical and systemic administrations of melatonin and dexamethasone on facial nerve regeneration. MATERIALS AND METHODS In total, 50 male albino Wistar rats underwent facial nerve axotomy and neurorrhaphy. The animals were divided into 5 groups: control, topical melatonin, systemic melatonin, topical dexamethasone, and systemic dexamethasone. Nerve conduction studies were performed preoperatively and at 3, 6, 9, and 12 weeks after drug administrations. Amplitude and latency of the compound muscle action potentials were recorded. Coapted facial nerves were investigated under light and electron microscopy. Nerve diameter, axon diameter, and myelin thickness were recorded quantitatively. RESULTS Amplitudes decreased and latencies increased in both the melatonin and dexamethasone groups. At the final examination, the electrophysiological evidence of facial nerve degeneration was not significantly different between the groups. Histopathological examinations revealed the largest nerve diameter in the melatonin groups, followed by the dexamethasone and control groups (p<0.05). Axon diameter of the control group was smaller than those of the melatonin (topical and systemic) and topical dexamethasone groups (p<0.05). The melatonin groups had almost normal myelin ultrastructure. CONCLUSION Electrophysiological evaluation did not reveal any potential benefit of dexamethasone and melatonin in contrast to histopathological examination, which revealed beneficial effects of melatonin in particular. These agents may increase the regeneration of facial nerves, but electrophysiological evidence of regeneration may appear later.

Investigation of the protective effects of crocin on acrylamide induced small and large intestine damage in rats

Abstract We investigated repair of acrylamide (AA) induced damage in intestines by administration of crocin. We used 40 male Wistar rats in four groups of 10 animals: control, AA, crocin, and AA + crocin groups. We investigated biochemical and histological changes to small and large intestine. AA ingestion decreased glutathione (GSH) levels and total antioxidant status (TAS) in the intestine compared to the control group, while superoxide dismutase (SOD) and catalase (CAT) activities, and total oxidant status (TOS) and malondialdehyde (MDA) levels were increased. Villi were shortened and villus degeneration was observed in ileum of the AA group. Degeneration of surface epithelium and Liberkühn crypts were observed in colon sections. GSH and TAS levels increased after administration of AA together with crocin, while SOD and CAT levels and TOS and MDA levels decreased; significant recovery of histological damage also was observed. We found that crocin exhibits protective effects on AA induced small and large intestine damage by inhibiting oxidative stress.

Thymoquinone is protective against 2,3,7,8-tetrachlorodibenzo-p-dioxin induced hepatotoxicity

Abstract We investigated changes in rat liver tissues following administration of thymoquinone (TQ) against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced hepatotoxicity. Fifty rats were assigned randomly to five groups of 10 as follows: control, corn oil, TCDD, TQ and TCDD + TQ. Biochemical and histopathological analyses were conducted on liver tissue. We found that 30 day TCDD administration caused histopathological changes in liver including thickening of Glisson’s capsule, intracytoplasmic vacuolization in hepatocytes, sinusoidal dilation, vascular and sinusoidal congestion and inflammatory cell infiltration. TCDD administration increased malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels in rat liver tissue and reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels compared to all other groups. In the TQ treated group, GSH, SOD, CAT and TAS levels increased compared to all other groups. MDA, TOS, ALT, AST, ALP levels decreased compared to all other groups. Our histological findings were consistent with the biochemical findings. The oxidative and histologic effects of TCDD were eliminated by TQ treatment. TCDD administration caused oxidative stress in rat liver and TQ administered with TCDD prevented TCDD induced hepatotoxicity. TQ could be considered an alternative anti-TCDD toxicity agent.