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Öğe Calpain inhibitor AK 295 inhibits calpain-induced apoptosis and damage in rat kidney(Scientific Publishers of India, 2018) Aydemira S.; Binena M.; Parlakpinar H.; Dilsiz N.Objectives: In the present investigation, the effect of a calpain inhibitor, AK 295, on ischemia/ reperfusion damage in rat kidney were investigated and evaluated. Materials and methods: 28 male Wistar Albino rats were separated into 4 main random groups (n=7), named group I (control), group II (ischemia-reperfusion), group III (AK295+ischemia-reperfusion) and group IV (DMSO+ischemia-reperfusion). Right kidney nephrectomy under anesthesia of xylazine (5 mg/kg) and ketamine (75 mg/kg) was performed to the rats except for group I. The rats under reversible general anesthesia underwent 30 min total ischemia and then, blood samples (5 cc) and kidney tissues were taken from all the groups rapidly. Caspase 3 enzyme activity was detected in the kidney tissues by Western-blot technique. Serum creatinine and urea values, amount of kidney malondialdehyde, and differences in the cellular antioxidant enzymes superoxide dismutase and catalase were also analyzed. Results: In AK295+IR group, caspase-3 enzyme band was not observed due to the fact that the calpain inhibitor AK295 prevented the ischemic damage. On the other hand, in DMSO+IR group, significant bands appeared due to apoptosis. It was also found that catalase levels in AK295+I/R and DMSO+I/R groups increased insignificantly compared to I/R group (p<0.05). Conclusions: As a result of the study, AK295 could provide further knowledge on ischemia-reperfusion damage that has no current treatment and it could have a place in ischemia-reperfusion damage treatment protocol. © 2018, Scientific Publishers of India. All rights reserved.Öğe Effects of dexmedetomidine and midazolam on motor coordination and analgesia: A comparative analysis(2013) Aydogan M.S.; Parlakpinar H.; Ali Erdogan M.; Yucel A.; Ucar M.; Sa?ir M.; Colak C.Objective: We compared the effects of 2 sedative drugs, dexmedetomidine and midazolam, on motor performance and analgesic efficacy in a rat model. Materials and methods: Rats were randomly divided into the following 4 groups on the basis of the treatment received. The first group received 83 ?g/kg/min midazolam; the second, 1 ?g/kg/min dexmedetomidine; the third, 83 ?g/kg/min morphine; and the fourth was a control group. The rats were measured motor coordination and pain reflexes by using rotarod, accelerod, hot plate, and tail flick tests. Results: At all the tested speeds, the midazolam-injected rats remained on the rotarod longer than did the dexmedetomidine-injected rats. Furthermore, in the 10-minute accelerod test, the midazolam-injected rats remained for a longer duration than did the dexmedetomidine-injected rats. The latency time for the hot plate test was significantly higher at 10 minutes and 20 minutes in the dexmedetomidine group than in the midazolam group. Further, the latency time at 10 minutes for the tail flick test was greater in the dexmedetomidine group than in the midazolam group. Conclusions: In this rat model, midazolam results in faster recovery of motor coordination performance when compared with dexmedetomidine. © 2013 The Authors.Öğe Effects of Perineural Administration of Dexmedetomidine in Combination with Levobupivacaine in a Rat Sciatic Nerve Block(2013) Ali Erdogan M.; Polat A.; Yucel A.; Aydogan M.S.; Parlakpinar H.; Tekin S.; Durmus M.Objective: The aim of this study was to assess if perineural administration of dexmedetomidine combined with levobupivacaine increases the duration of the sensory and motor blockade of a sciatic peripheral nerve block in rats. Methods: Forty male Sprague-Dawley rats were randomly divided into 5 experimental groups: Group 1, sham; Group 2, perineural levobupivacaine (0.2 mL of a 0.5% solution) and subcutaneous saline; Group 3, perineural levobupivacaine (0.2 mL of a 0.5% solution) plus dexmedetomidine (20 ?g/kg dexmedetomidine) and subcutaneous saline; Group 4, perineural saline and subcutaneous dexmedetomidine; and Group 5, perineural saline and subcutaneous saline. Pain reflexes in response to a thermal stimulus were measured at 0 and 240 minutes after drug administration by using a hot-plate and tail-flick tests. Neurobehavioral status, including sensory and motor functions, was assessed by an investigator who was blinded to the experimental groups every 30 minutes until normal functioning resumed. Results: The sensory and motor blockades of the rats did not increase in the treatment with dexmedetomidine plus levobupivacaine when compared with the treatment with levobupivacaine alone at all the time points ( P > 0.05). Compared with rats in Group 2, those in Group 3 showed significantly higher latency times at 30 and 60 minutes in the hot plate test ( P < 0.01). At 30 and 60 minutes, the latency times of the rats in Group 3 were longer than those in Group 2 in the tail-flick test ( P < 0.01). Furthermore, the durations of the complete sensory and motor blockade were similar when treatment with levobupivacaine plus dexmedetomidine was compared with treatment with levobupivacaine alone. Conclusions: A 20?g/kg dose of dexmedetomidine added to levobupivacaine did not increase the duration of the sensory and motor blockades in rats. However, treatment with dexmedetomidine plus levobupivacaine increased the quality of analgesia in rats. © 2013 The Authors.Öğe An investigation of the effects of duloxetine on the heart(OrtadogŸu Reklam Tanitim Yayincilik Turizm Egitim Insaat Sanayi ve Ticaret A.S., 2020) Eranil I.; Vardi N.; Yildiz A.; Parlakpinar H.; Özhan O.Objevtive: The present study was designed to examine the effects of high dose and low dose duloxetine on Cx43, a gap junction (GJ) protein; on S100A, cardiac contractility component and on certain early cardiac impairment parameters as TnI and TnT. Material and Methods: The study was performed with 24 male Wistar Albino rats by generating control group (1 ml solvent), low-dose duloxetine (LDD) group (10 mg/kg) and high-dose duloxetine (HDD) group (100 mg/kg). After the experimental procedure, the results concerning blood pressure and heart rates of the anesthetized rats were recorded and HE staining and immunostaining of Cx43, S100A, TnI and TnT were applied to the heart tissue sections. Results: In the control group, Cx43 was stained as marked streaks between cardiomyocytes; TnI, TnT and S100A were stained as homogenous and dark brown in cytoplasm. Nevertheless, intensity of Cx43 immunostaining showed significant increase in duloxetine- treated groups (p<0.001). TnT (p=0.024, p=0.004, p<0.05) and S100A (p<0.001) immunostaining were low in high dose group compared to control group and low dose group. TnI immunostaining also demonstrated significant decrease in high dose duloxetine group as compared to the control group (p<0.001). There was no statistically significant difference between groups in terms of heart rate, ECG parameters, MDA, SOD, GSH and CAT levels (p>0.05). Conclusion: Our study reveals that duloxetine induced an increase in the immunostaining of Cx43, and a decrease in the immunostaining of TnI, TnT and S100A, also known as early cardiac parameters. Furthermore, duloxetine was observed to show no effect on oxidant and antioxidant parameters. While heart rate remained unchanged, mean blood pressure decreased in high dose duloxetine group. In the light of the study outcomes, it has been concluded that antidepressants must be administered more advertently in depression patients with heart disorders. © 2020 by Türkiye Klinikleri. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Öğe Overview of the cell death; Comparison of necrosis and apoptosis(2003) Parlakpinar H.; Koç M.; Acet A.There are two distinct forms of cell death; necrosis and apoptosis. Necrosis is the traumatical cell death that occurs after physical and chemical factors. Apoptosis is the genetically regulated cell death that permits the safe disposal of cells when they are damaged or completed their intended biological function. There are many differences between necrosis and apoptosis including biochemical and morphological changes. Finally, knowledge of molecular mechanisms of apoptosis provides insights into the causes of multiple abnormalities involving in the regulation of aberrant cell death and encourages new approches for the treatment of human diseases.Öğe The protective effect of aminoguanidine on random pattern skin flap survival: An experimental study in rats(Turkiye Klinikleri, 2007) Aydo?an H.; Gürlek A.; Parlakpinar H.; Aydo?an N.; Acet A.Objective: Distal flap necrosis resulting from ischemia is a serious problem, and increases the cost of treatment. Reactive oxygen radicals (ROS) play an important role in tissue injury and ischemia, and may lead to partial or complete flap necrosis. Aminoguanidine (AG), a potent antioxidant, prevents ROS formation and lipid peroxidation. Besides, AG inhibits inducible nitric oxide synthase (iNOS) leading to decreased generation of nitric oxide (NO). Material and Methods: Rats were randomly divided into three groups: Control, flap elevated saline group, and AG treated group, A caudally based rectangular flap, 3 x 10-cm was elevated on the back of the rats. Flap viability was evaluated 7 days after the initial operation, measuring necrotic areas and total flap areas by computer-assisted planimetry. Malondialdehyde (MDA), NO, glutathione (GSH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) levels were measured in flap skin tissue to observe the effects of AG. Results: Rate of flap necrosis and MDA, NO levels were higher in the saline group compared to the control group, while GSH, GSH-Px, and SOD enzyme activities were reduced. AG administration reduced lipid peroxidation, NO generation and increased GSH, GSH-Px, SOD enzyme activities. Furthermore, it significantly reduced the rate of flap necrosis when compared with the saline group. Conclusion: We believe that AG, a potent antioxidant and iNOS inhibitor, has beneficial effects to improve skin flap viability when distal flap necrosis is a potential complication in longer flaps. Copyright © 2007 by Türkiye Klinikleri.Öğe The protective effect of N-acetylcysteine amide against paraquat-induced neurotoxicity(TUBITAK, 2019) Ateş B.; Vardi N.; Parlakpinar H.; Karaaslan M.G.; Yilmaz İ.; Ercal N.N-acetylcysteine amide (NACA) is a new antioxidant molecule with powerful radical scavenging properties. The aim of this study was to investigate neuroprotective effects of NACA against paraquat (PQ) toxicity in the midbrains of rats by using motor coordination tests and biochemical and histological analysis. Thirty adult Wistar albino rats were divided into three groups: Group 1: control (n = 10), Group 2: PQ (10 mg/kg) (n = 10), and Group 3: PQ (10 mg/kg) + NACA (100 mg/kg) (n = 10). NACA was administrated intraperitoneally 30 min before PQ injection. Performance was measured for a period of 28 days. The rotarod and accelerod tests were performed prior to and after the experimental period. After the experimental period, rats were sacrificed and midbrain tissues were removed. According to biochemical data, malondialdehyde levels exhibited a significant increase (P <0.05) when the PQ group was compared to the control group, whereas the NACA-treated group showed a significant decline (P < 0.05). The total glutathione levels (P < 0.01) and the glutathione peroxidase and butyrylcholinesterase activities (P < 0.05) in the NACA treatment group were significantly raised compared with the PQ group. The main finding in the rotarod and accelerod tests was that the PQ+NACA group had improved motor coordination functions, whereas the PQ group had lost motor coordination (P < 0.05). Our histological data were also outstanding and were consistent with biochemical and motor coordination results in terms of the protective role of NACA against PQ-induced neurotoxicity. © TÜBİTAKÖğe Protective effects of melatonin and ?-D-Glucan against liver injury in rats - A comparative study(Wroclaw University of Medicine, 2013) Aydogan M.S.; Erdogan M.A.; Polat A.; Yücel A.; Ozgül U.; Parlakpinar H.; Duran Z.R.Objectives. The aim of this study was to investigate the possible protective effects of melatonin and ?-D-glucan against ischemia-reperfusion (IR) injury in rats. Materials and Methods. Forty rats were randomly divided into 5 groups, each consisting of 8 animals, as follows. Sham group [S], IR group [C], IR + ?-Glucan group [?], IR + melatonin group [MLT], IR + melatonin + ?-Glucan group [MLT + ?]. The rats in the C, ?, MLT and MLT + ? groups were subjected to IR for 60 min each. Melatonin (10 mg·kg-1) was intraperitoneally injected for a single dose 30 min before IR. ?-Glucan (50 mg·kg-1·day -1) was orally administered for 10 days to rats. All of the rats were killed on day 11, and histological changes in the liver and tissue levels of oxidants and antioxidants were evaluated. Results. Malondialdehyde [MDA] level were significantly higher in the C group compared to the S group (p = 0.007). MDA level were significantly higher in the ? group compared to the MLT and MLT + ? groups (p =0.007). Tissue antioxidant markers (superoxide dismut ase [SOD], glutathione-peroxidase [GPx], and catalase [CAT]) were significantly lower in the C group than the S group (p < 0.05). SOD levels were simply not significant in the < group compared to the MLT and MLT + < groups. CAT and GPx activities were significantly higher in the ? group compared to the MLT and MLT + ? groups (p = 0.004).The histological damage ameliorated in ?, MLT and MLT + ? groups compared to C group. Conclusion. Our results suggest that melatonin and P-glucan combination pretreatment suppressed oxidative stress and increased antioxidant levels in an experimental rat model of liver IR injury. © Copyright by Wroclaw Medical University.
