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Öğe Effect of thymoquinone on NRF2/NF-kB/MAPK pathway in methotrexate-induced rat testis injury(Mashhad Univ Med Sciences, 2024) Kaymak, Emin; Ceylan, Tayfun; Akin, Tugrul; Kuloglu, Nurhan; Sayan, Meryem; Degen, Necla; Onal, EsraObjective(s): In this study, we aimed to investigate the protective effect of Thymoquinone (THQ) against testicular damage caused by Methotrexate (MTX). Materials and Methods: This study consists of 5 groups: Control, Olive oil, THQ, MTX, and MTX+THQ. At the end of the experiment, spermiogram analysis was performed on the rats. In addition, testicular tissues were taken and histopathology, immunohistochemistry, and biochemistry analysis were performed. Biochemical analyses were performed on the serums. Results: According to the results obtained, spermiogram values, Johnson's testicular biopsy score, SOD, CAT, GPx, FSH, LH, and testosterone values were statistically significantly decreased in the MTX group compared to the control group. In the MTX+THQ group, spermiogram values, Johnson's testicular biopsy score, SOD, CAT, GPx, FSH, LH, and testosterone values increased statistically significantly compared to the MTX group. NRF2 and HO-1 immunoreactivity were statistically significantly decreased in the MTX group compared to the control group. In the MTX+THQ group, NRF2 and HO-1 immunoreactivity were statistically significantly increased compared to the MTX group. The level of MDA, which is important in lipid damage, and the level of biochemistry results of TNF-alpha, IL1-beta, and IL-6, which are important markers, and the results of p-NF-kB and P38 immunoreactivity were statistically significantly increased in the MTX group compared to the control group. In the MTX+THQ group, these parameters showed a significant decrease compared to the MTX group. Conclusion: According to these results, it is thought that THQ will play a protective role against infertility caused by chemotherapy-induced testicular damage.Öğe Effect of vitamin B12 on methotrexate-induced cardiotoxicity in rats(Mashhad Univ Med Sciences, 2024) Kuloglu, Nurhan; Karabulut, Derya; Kaymak, Emin; Akin, Ali Tugrul; Ceylan, Tayfun; Yildirim, Aysegul Burcin; Yakan, BirkanObjective(s): Methotrexate (MTX) is a drug with anti-inflammatory and immunosuppressive effects and is also a folic acid antagonist. Our aim in this study is to determine the molecular mechanisms of cardiotoxicity caused by MTX, a chemotherapeutic drug, and to evaluate the protective effects of vitamin B12 on this toxicity. Materials and Methods: A total of 32 rats were used in our study and 4 groups were formed. Control group, Vit B12 group (3 mu g/kg B12 for 15 days, IP), MTX group (20 mg/kg MTX single dose on day 8 of the experiment, IP), MTX +Vit B12 group (3 mu g/kg, IP ), Vit B12 throughout the 15 days, and a single dose of 20 mg/kg MTX (IP) on day 8 of the experiment. Immunohistochemically, expressions of hypoxia-inducible factor 1 alpha (HIF1-alpha), vascular endothelial growth factor receptor -2 (VEGFR-2), erythropoietin (EPO), and interleukin-6 (IL -6) were evaluated in the heart tissue. Total catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were measured in the heart tissue. At the same time, ANP and NT-proBNP levels were measured in the blood serum. Results: In the study, the expression of HIF1-alpha and VEGFR-2 increased significantly in the MTX group, while IL -6 and EPO significantly decreased. At the same time, CAT and SOD levels were significantly decreased and MDA levels increased significantly in the MTX group. While vitamin B12 significantly corrected all these values, it also greatly reduced the increases in ANP and NT-proBNP levels caused by MTX. Conclusion: It is important to use Vit B12 before and after MTX administration to replace the folate that MTX has reduced.Öğe Effects of vitamin B12 on methotrexate hepatotoxicity: evaluation of receptor-interacting protein (RIP) kinase(Springer, 2020) Karabulut, Derya; Ozturk, Emel; Kuloglu, Nurhan; Akin, Ali Tugrul; Kaymak, Emin; Yakan, BirkanIn the study, we aimed to show the effects of vitamin B12 on the necrosis caused by methotrexate (MTX), a folic acid antagonist. Thirty-two rats were randomly assigned to four groups of eight rats per group. Control (n= 8), Vit B12 (n= 8) 3 mu g/kg/ip B12 (15 days) per day throughout the experiment, MTX (n= 8) injected with a single dose of 20 mg/kg/ip MTX on 8th day of experiment, MTX + Vit B12 (n= 8) injected with a single dose of 20 mg/kg ip methotrexate on 8th day of experiment + 3 mu g/kg/ip Vit B12 (15 days) per day throughout the experiment. Oxidant (TOS)/antioxidant (TAS) system, TNF-alpha and TGF-beta levels, AST and ALT, serum vitamin B12 levels were determined in the tissue. Cyclooxygenase-2 (Cox-2), receptor-interacting protein kinase 1 (RIP1) and 3 (RIP3) immunohistochemistry were applied to the liver tissue. TOS increased; TAS decreased; TNF-alpha and TGF-beta levels increased; AST and ALT levels changed after MTX hepatotoxicity. Vit B12 decreased significantly. COX-2, RIP1, and RIP3 immunoreactivity increased. Vit B12 showed improvement in all of the negative results. Vit B12 is an important supplement to be used against necrosis in tissue after MTX hepatotoxicity.Öğe HISTOPATHOLOGICAL CHANGES IN LUNG TISSUE CAUSED BY DIABETES: A REVIEW(Dokuz Eylul Univ Inst Health Sciences, 2023) Yildirim, Aysegul Burcin; Karabulut, Derya; Kaymak, Emin; Kuloglu, Nurhan; Akin, Ali Tugrul; Ceylan, Tayfun; Ozturk, EmelDiabetes mellitus (DM) associated with oxidative stress and inflammation can affect many organs. While the effects of diabetes on many organs are well known and documented, its mechanisms of action on the lung are known far less. Hyperglycemia can lead to lung damage by increasing oxidative stresses and inflammation. Diabetes may be a trigger for pulmonary fibrosis, as studies suggest that there may be an important link between pulmonary fibrosis and diabetes. In this review, the histopathological changes caused by diabetes in the lung tissue were summarized. In addition, changes in the lung due to inflammation, oxidative stress and pulmonary fibrosis mechanisms were evaluated.Öğe Investigation of the effect of Myricetin on Cisplatin-induced liver hepatotoxicity(Assoc Medica Brasileira, 2024) Aksoy, Suemeyye; Kuloglu, Nurhan; Karabulut, Derya; Yakan, BirkanOBJECTIVE: Cisplatin, a widely used anticancer agent, induces hepatotoxicity alongside organ damage. Understanding Cisplatin's toxicity mechanism and developing preventive measures are crucial. Our study explores Myricetin, a flavonoid, for its protective effects against Cisplatin-induced hepatotoxicity. METHODS: In our study, a total of 32 Wistar albino male rats were utilized, which were categorized into four distinct groups: Control, Myricetin, Cisplatin, and Myricetin+Cisplatin. For the histological assessment of hepatic tissues, hematoxylin-eosin and periodic acid Schiff staining were employed, alongside immunohistochemical measurements of TNF-alpha, alpha, interleukin-17, and interleukin-6 immunoreactivity. Additionally, aspartate transaminase and alanine transaminase values were examined by biochemical analysis. RESULTS: In the histological evaluation of the tissues, a normal healthy cell structure and a strong periodic acid Schiff (+) reaction were observed in the hepatocyte cells in the tissues of the Control and Myricetin groups, while intense eosinophilia, minimal vacuolization, congestion, and sinusoidal expansions were observed in the hematoxylin-eosin stainings, and a decrease in the positive reaction in the periodic acid Schiff staining was observed in the Cisplatin group. Consistent with these histological findings, an increase in TNF-alpha, alpha, interleukin-17, and interleukin-6 expressions (p<0.0001) and a concomitant increase in aspartate transaminase and alanine transaminase values were observed in the Cisplatin group. In the group protected by Myricetin, a significant improvement was observed in all these histological and biochemical values. CONCLUSION: Cisplatin induces notable histopathological alterations in the liver. In this context, Myricetin exhibits the potential to alleviate Cisplatininduced damage by modulating histological parameters and biochemical processes.Öğe Investigation of the Therapeutic Effects of Chloroquine in Adriamycin-Induced Hepatotoxicity(Sciendo, 2021) Akin, Ali Tugrul; Kaymak, Emin; Ozturk, Emel; Karabulut, Derya; Kuloglu, Nurhan; Ceylan, Tayfun; Toluk, AyseThe aim of this study is to investigate the therapeutic effects of Chloroquine (CLQ) against Adriamycin (ADR) induced hepato-toxicity. ADR is a chemotherapeutic agent used in the treatment of many cancer types, but it causes hepatotoxicity. CLQ is used as an anti-inflammatory drug in the treatment of malaria, rheumatoid arthritis, and pneumonia caused by Covid-19. Rats were divided into four groups: Control group, ADR group (2 mg/kg Adriamycin, one in three days for 30 days, i.p.), CLQ group (50 mg/kg Chloroquine, per day for 30 days, i.p.), ADR+CLQ (2 mg/kg Adriamycin, one in three days for 30 days, i.p. and 50 mg/kg Chloroquine, per day for 30 days, i.p.). Animals were sacrificed, and liver tissues were extracted for further examinations. Histopathological changes in liver tissues were scored and IL-17 immunostaining was performed to determine the expression levels among experimental groups. Bodyweights in the ADR group decreased significantly compared to the Control group and CLQ group. Furthermore, bodyweight in ADR+CLQ group was significantly higher compared to ADR group. The histopathological score was significantly higher in ADR group when compared to Control and CLQ group while CLQ administrations reduced the damage induced by ADR in the ADR+CLQ group. IL-17 immunoreactivity was considerably increased in the ADR group. On the other hand, IL-17 expressions of ADR+CLQ were substantially less compared to ADR group. We suggest that CLQ can be used as a therapeutic agent to reduce the detrimental effects of ADR, thanks to its anti-inflammatory properties.Öğe Investigation of vascular endothelial growth factor receptor-dependent neuroplasticity on rat nucleus tractus solitarius and phrenic nerve after chronic sustained hypoxia(Wiley, 2021) Kuloglu, Nurhan; Basaran, Kemal E.; Yakan, BirkanThe neuronal system that controls respiration creates plasticity in response to physiological changes. Chronic sustained hypoxia causes neuroplasticity that contributes to ventilatory acclimatization to hypoxia (VAH). The purpose of this study is to explain the potential roles of the VAH mechanism developing because of chronic sustained hypoxia on respiratory neuroplasticity of vascular endothelial growth factor (VEGF) receptor activation on the nucleus tractus solitarius (NTS) and phrenic nerve. In this study 24 adult male Sprague-Dawley rats were used. Subjects were separated into four groups, a moderate-sham (mSHAM), severed-sham (sSHAM), moderate chronic sustained hypoxia (mCSH), and severed chronic sustained hypoxia (sCSH). Normoxic group (mSHAM and sSHAM) rats were exposed to 21% O-2 level (7 days) in the normobaric room while hypoxia group (mCSH and sCSH) rats were exposed to 13% and 10% O-2 level (7 days). Different protocols were applied for normoxic and hypoxia groups and ventilation, respiratory frequency, and tidal volume measurements were made with whole-body plethysmography. After the test HIF-1 alpha, erythropoietin (EPO), and VEGFR-2 expressions on the NTS region in the medulla oblongata and phrenic nerve motor neurons in spinal cord tissue were analyzed using the immunohistochemical stain method. Examinations on the medulla oblongata and spinal cord tissues revealed that HIF-1 alpha, EPO, and VEGFR-2 expressions increased in hypoxia groups compared to normoxic groups while a similar increase was also seen when respiratory parameters were assessed. Consequently, learning about VAH-related neuroplasticity mechanisms developed as a result of chronic continuous hypoxia will contribute to developing new therapeutical approaches to various diseases causing respiratory failure using brain plasticity without recourse to medicines.Öğe Protective effect of melatonin on cisplatin induced acute kidney injury: Role of regulation of heat shock proteins expressions(Natl Inst Science Communication-Niscair, 2023) Akin, Ali Tugrul; Unsal, Murat; Ceylan, Tayfun; Kaymak, Emin; Ozturk, Emel; Kuloglu, Nurhan; Karabulut, DeryaChemotherapy is one of the major treatment approaches for cancer, and these agents are known to cause severe side effects, including damaging vital organs. Cisplatin (CP) is a commonly used chemotherapeutic agent in the treatment of many cancer types, particularly lung, breast, ovarian, testicular and head-neck cancers. CP is reported to cause damage to damage on brain, kidney, liver and gonads. In this study, is we investigated the protective effects of melatonin (MEL) in acute kidney injury (AKI) induced by CP via assessment of heat-shock protein (HSP) induction in rats. For this purpose, total 40 Wistar albino rats were divided into four groups: Control (n=10), MEL (n=10, 10 mg/kg/i.p. melatonin for 8 days), CP (n=10, 7 mg/kg/i.p. cisplatin at the 5th day), and CP+MEL (n=10, 10 mg/kg/i.p. melatonin for 8 days and 7 mg/kg/i.p. cisplatin at the 5th day). After kidney tissues were extracted, histopathological changes were evaluated and immunoreactivities of HSP47, HSP60, HSP70 and HSP90 in renal cortex were detected via immunohistochemistry. Moreover, blood serum BUN (blood urea nitrogen), creatinine and uric acid levels were measured to assess kidney function. CP group showed histopathological deterioration, and MEL treatment attenuated this damage in CP+MEL group. An increase in HSPs immunoreactivities were detected in renal cortex of CP group when compared with the control and MEL groups, showing increased HSP response because of CP-induced AKI. However, CP-induced HSP induction was significantly lower in the CP+MEL group. Similarly, blood serum BUN, creatinine and uric acid levels were higher in CP group while CP+MEL group showed decreased levels of these parameters. Our results suggest that MEL could exert a significant protective effect against CP-induced AKI via reducing HSP response.Öğe Response to chronic sustained hypoxia: increased cytosolic gelsolin and decreased plasma gelsolin levels(Springer, 2024) Gunturk, Inayet; Kuloglu, Nurhan; Seydel, Gonul Seyda; Yazici, Cevat; Basaran, Kemal Erdem; Yakan, Birkan; Karabulut, DeryaAn actin binding protein, gelsolin (GSN) has two isoforms, plasma (pGSN) and cytosolic (cGSN). Changes in pGSN and/or cGSN levels have been shown to be associated with the pathogenesis of several diseases. The aim of this study was to evaluate changes in intracellular and extracellular GSNlevels with HIF-1 in animals exposed to chronic sustained hypoxia (CSH), in addition to apoptosis and the cellular redox status. The rats in the Sham group were exposed to 21% O-2, and the rats in the hypoxia groups were exposed to 13 and 10% O-2, respectively. Plasma pGSN, HIF-1 alpha, Total Antioxidant Status (TAS) and Total Oxidant Status (TOS), and lung tissue pGSN, HIF-1 alpha, TAS, TOS, GSN levels, and apoptotic cell numbers were measured. HIF-1 alpha levels were found to increase significantly in the tissue, especially in the group with severe hypoxia, both in biochemical and histological examinations. pGSN levels were also significantly decreased in both plasma and tissue. Significant increases in tissue were observed in cGSN. It was observed that while the antioxidant activity was dominant in the tissue, the oxidant activity was dominant in the plasma. In particular, the response to hypoxia regulated by HIF-1 is very important for cellular survival. The results of this study showed that the increase in cGSN and TAS levels in the lung tissue together with HIF-1 alpha can be considered as the activation of mechanisms for cellular protection.Öğe Thymoquinone reduces methotrexate-induced heart damage: a histopathological study in rats(Cukurova Univ, Fac Medicine, 2023) Yildirim, Aysegul Burcin; Kaymak, Emin; Ceylan, Tayfun; Akin, Ali Tugrul; Kuloglu, Nurhan; Sayan, Meryem; Deger, NeclaPurpose: The study aimed to evaluate the effect of thymoquinone on cardiac tissue in MTX-induced cardiac toxicity in rats with various parameters.Materials and Methods: Group I (n=8) was administered intraperitoneal saline for 10 days. Intraperitoneal olive oil was applied to Group II (n=8) for 10 days. Group III (n=8) received 10 mg/kg Thymoquinone (THQ) intraperitoneally for 10 days. Group IV (n=8) was administered a single dose of 20 mg/kg Methotrexate (MTX), 500 mg/20 ml, intraperitoneally on the 1st day of the experiment. Group V (n=8) MTX: 20 mg/kg single dose intraperitoneally on the 1st day; THQ: 10mg/kg i.p. administered for 10 days. Since Methotrexate was in liquid form, no solvent was used. At the end of the experimental period, the rats were sacrificed for analysis of heart tissue. The structure of heart tissue was evaluated by hematoxylin-eosin staining. Immunohistochemically, Connexin-43, HSP90, and HIF- 1 alpha antibodies were stained.Results: Group IV was found to have histopathological deterioration, which was ameliorated by THQ. In addition to this; Connexin-43 immunoreactivity was the lowest in Group IV compared to other groups: 108.5 +/- 7.4. Compared to other groups, HSP90 immunoreactivity was highest in Group IV: 103.6 +/- 10.4. Compared to other groups, HIF-1 alpha immunoreactivity was highest in Group IV: 95.2 +/- 9.1.Conclusion: Thymoquinone has a positive effect on Connexin-43, one of the proteins providing conduction in intercalary discs, HSP90, one of the chaperones in the cell and HIF-1 alpha expression against MTX toxicity. At the same time, THQ provides a significant improvement in cardiac tissue histopathologically by showing a cardioprotective effect.Öğe Vitamin B12 suppresses GADD153, prevents apoptosis and regulates the testicular function in methotrexate treated rat testis(Taylor & Francis Ltd, 2022) Karabulut, Derya; Ozturk, Emel; Kaymak, Emin; Kuloglu, Nurhan; Akin, Ali Tugrul; Yakan, BirkanMethotrexate (MTX) is an anti-neoplastic drug that also causes testicular damage. Vitamin B12 (Vit B12) is a water soluble vitamin that is required for normal metabolism. We investigated Vit B12 as a possible protective agent against testicular damage caused by MTX treatment. We divided rats into four groups: control group, Vit B12 group treated with Vit B12 daily for 15 days, MTX group treated with MTX on day 8, MTX + Vit B12 group treated with MTX on day 8 + Vit B12 for 15 days. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone were measured. We also measured proliferating cell nuclear antigen (PCNA), connexin43 (Cx43) and the growth arrest- and DNA damage-inducible gene, 153 (GADD153), using immunohistochemical staining. Apoptosis was assessed using TUNEL staining. The MTX group exhibited degeneration of seminiferous tubules; decreased serum testosterone, LH and FSH levels; fewer PCNA positive cells; increased Cx43 expression; and increased GADD153 and TUNEL stained cells compared to the control group. These pathologic findings were substantially reversed In the MTX + Vit B12 group. MTX caused increased endoplasmic reticulum stress and apoptosis via GADD153. Consequently, Vit B12 potentially is a protective agent against damage caused by MTX.
