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    Alpha B-crystallin Ameliorates Imbalance of Redox Homeostasis, Inflammation and Apoptosis in an Acute Lung Injury Model with Rats
    (Galenos Publ House, 2024) Kocak, Seda; Guner, Ibrahim; Yaman, Muhittin Onur; Yilmaz, Tugba E. K. I. Z.; Guzel Meydanli, Emine Elif; Yelmen, Nermin; Sahin, Gulderen
    Objective: Ischemia-reperfusion (IR) of the aorta is a significant contributor to the development of postoperative acute lung damage after abdominal aortic surgery. The aim of the present study was to examine the effect of alpha B-crystallin, a small heat shock protein (known as HspB5), on lung injury induced by abdominal aortic IR in rats. Methods: Male Sprague-Dawley rats were divided into three groups: control, ischemia-reperfusion (IR, 90 min ischemia and 180 min reperfusion), and alpha B-crystallin +IR. Alpha B-crystallin (50 mu g/100 g) was intraperitoneally administered 1 h before IR. Lung tissue samples were obtained for histological and biochemical analyses of oxidative stress and cytokine and apoptosis parameters in plasma, lung tissues, and bronchoalveolar lavage (BAL) fluid. Results: The levels of malondialdehyde, reactive oxygen species, total oxidant status, tumor necrosis factor-alpha (TNF-a), interleukin-1 beta (IL-1(3), nuclear factor kappa B (NFK(3), caspase-9 (CASP-9), 8-hydroxy2'-deoxyguanosine, total antioxidant status, superoxide dismutase, and interleukin-1 0 levels in lung tissues, plasma, and BAL fluid (p<0.0 5 versus control) increased in Aortic IR. However, alpha B-crystallin significantly reduced the lung tissue levels of oxidative, inflamatuvar, and apoptotic parameters in the plasma, lung tissues, and BAL fluid (p<0.05 versus aortic IR). Histopathological results showed that alpha B-crystallin ameliorated the morphological changes related to lung injury (p<0.001). Conclusion: Alpha Alpha B-crystallin substantially restored disrupted the redox balance, inflammation, and apoptotic parameters in rats exposed to IR. The cytoprotective effect of alpha B-crystallin on redox balance might be attributed to improved lung injury.
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    Aortic Injury via Ischemia Reperfusion and the Preventive Role of Fluoxetine
    (Wiley, 2023) Yaman, Muhittin Onur; Altan, Mehmet; Kervancıoğlu, Elif Demirci; Kılıç, Aysu; Kervancıoğlu, Gülnaz; Polat, Sila Hidayet Bozdoğan; Karadeniz, Zeliha
    [Abstract Not Available]
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    Aortic ischemia-reperfusion injury and potency of fluoxetine
    (Mashhad Univ Med Sciences, 2023) Altan, Mehmet; Yaman, Muhittin Onur; Kervancıoğlu, Gülnaz; Kılıç, Aysu; Demirci, Elif Kervancıoğlu; Polat, Sila Hidayet Bozdoğan; Karadeniz, Zeliha
    Objective(s): Due to cross-clamping of the aorta during aortic aneurysm surgeries, ischemia-reperfusion (IR) develops, and it may cause damage to the aorta itself or even to remote organs by oxidative stress or inflammation. Fluoxetine (FLX) which might be used in the preoperative period for its tranquilizing effect also has antioxidant effects in short-term use. The purpose of our study is to examine whether FLX protects aorta tissue, against the damage caused by IR. Materials and Methods: Three groups of Wistar rats were formed randomly. 1) Control group (sham -operated), 2) IR group (60 min ischemia+120 min perfusion), and 3) FLX+IR group (FLX dose was 20 mg/kg for 3 days IP before IR). At the end of each procedure, aorta samples were collected, and oxidant-antioxidant, anti-inflammatory, and anti-apoptotic status of the aorta were evaluated. Histological examinations of the samples were provided. Results: Levels of LOOH, MDA, ROS, TOS, MPO, TNF alpha, IL-1 beta, IL-6, NF-kB, MMP-9, caspase-9, 8-OHdG, NO, and HA were found to be significantly increased in the IR group compared with control (P<0.05) and SOD, GSH, TAS, and IL-10 levels were significantly lower (P<0.05). FLX significantly decreased LOOH, MDA, ROS, TOS, MPO, TNF alpha, IL-1 beta, IL-6, NF-kB, MMP-9, caspase-9, 8-OHdG, NO, and HA levels in the FLX+IR group compared with IR group (P<0.05) and increased IL-10, SOD, GSH, and TAS (P<0.05). FLX administration prevented the deterioration of aortic tissue damage. Conclusion: Our study is the first study that demonstrates FLX-mediated suppression of IR injury in the infrarenal abdominal aorta by antioxidant, anti-inflammatory, and anti-apoptotic properties.
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    The role of NMDA glutamate receptors in lung injury caused by chronic long-term intermittent hypobaric hypoxia
    (Assoc Bras Divulg Cientifica, 2023) Yaman, Muhittin Onur; Sönmez, O. F.; Ekiz-Yılmaz, T.; Sönmez, D.; Meydanlı, E. E. G.; Güner, İbrahim; Şahin, G.
    Chronic intermittent hypoxia (CIH), a component of sleep apnea-hypopnea syndrome, is suggested to cause damage to lung tissue, and the role of glutamate is not well studied. We used a chronic long-term intermittent hypobaric hypoxia (CLTIHH) model of rats to find out if such procedure causes lung injury and the potential effect of N-methyl-D-aspartate receptors (NMDARs) by using receptor antagonist MK-801 (dizocilpine). Thirty-two rats were placed into four groups; a control and three CLTIHH groups where rats were placed into a low-pressure chamber set to 430 mmHg for 5 h/day, 5 days/week, for 5 weeks. Only one group received MK-801 (0.3 mg/kg, ip) daily. We evaluated tumor necrosis factor (TNF)-a, interleukin (IL)-6, IL-10, and nuclear factor (NF)-kB for the inflammatory process, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GPX), total antioxidant status (TAS), and total oxidant status (TOS) for oxidative stress, and caspase-9 levels. Blood plasma, bronchoalveolar fluid (BALF), and lung tissue extracts were evaluated. Both oxidant and inflammatory parameters were significantly increased in all the mediums of the CLTIHH groups except the group that received MK-801. Significant evidence was collected on MK-801 alleviating the effect of CLTIHH. Histological evaluations revealed lung damage and fibrotic changes in the CLTIHH groups. It was first shown that the CLTIHH procedure caused chronic lung injury, and that inflammation and oxidant stress were influential in the formation of lung injury. Secondly, NMDAR antagonist MK-801 effectively inhibited the development of lung injury and fibrosis.