Browsing by Author "Erkan, Leman Gizem"

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    The acute cardiorespiratory effects of centrally injected arachidonic acid; the mediation of prostaglandin E, D and F-2 alpha
    (Elsevier, 2017-04-18) Erkan, Leman Gizem; Altınbaş, Burçin; Güvenç, Gökçen; Aydın, Begüm; Niaz, Nasir; Yalçın, Murat; Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0002-5600-8162; AAR-6815-2021; AAC-4975-2022; AAG-6956-2021; 56529371200; 55356919300; 56529426800; 57194022849; 57060367600; 57192959734
    Arachidonic acid (AA), which is released from synaptic membrane phospholipid by neuroreceptor-initiated activation of phospholipase A(2), is abundant in the brain and works as a neurotransmitter and/or neuromodulator in the central nervous system. Recently we reported that centrally injected AA generated pressor and hyperventilation effects by activating thromboxane A(2) (TXA(2)) signaling pathway. The present study was designed to investigate the mediation of other metabolites of AA such as prostaglandin (PG) D, PGE and PGF(2 alpha), alongside TXA(2) in the AA-evoked cardiorespiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA caused pressor, bradycardic and hyperventilation responses by increasing pO(2) and decreasing pCO(2) in adult male anaesthetized Sprague Dawley rats. Pretreatment (i.c.v) with different doses of DP/EP prostanoid receptor antagonist, AH6809 or FP prostanoid receptor antagonist, PGF(2 alpha), dimethylamine partially blocked the cardiorespiratory and blood gas changes induced by AA. In conclusion, these data plainly report that central PGD, PGE or PGF(2 alpha) might mediate, at least partly, centrally administered AA-evoked cardiorespiratory and blood gas responses.
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    The effects of centrally injected arachidonic acid on respiratory system: Involvement of cyclooxygenase to thromboxane signaling pathway
    (Elsevier, 2015-12-31) Erkan, Leman Gizem; Güvenç, Gökçen; Altınbaş, Burçin; Niaz, Nasır; Yalçın, Murat; Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0002-5600-8162; AAR-6815-2021; AAG-6956-2021; 56529371200; 56529426800; 55356919300; 57060367600; 57192959734
    Arachidonic acid (AA) is a polyunsaturated fatty acid that is present in the phospholipids of the cell membranes of the body and is abundant in the brain. Exogenously administered AA has been shown to affect brain metabolism and to exhibit cardiovascular and neuroendocrine actions. However, little is known regarding its respiratory actions and/or central mechanism of its respiratory effects. Therefore, the present study was designed to investigate the possible effects of centrally injected AA on respiratory system and the mediation of the central cyclooxygenase (COX) to thromboxane A2 (TXA2) signaling pathway on AA-induced respiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA induced dose- and time-dependent increase in tidal volume, respiratory rates and respiratory minute ventilation and also caused an increase in partial oxygen pressure (pO2) and decrease in partial carbon dioxide pressure (pCO2) in male anaesthetized Sprague Dawley rats. I.c.v. pretreatment with ibuprofen, a non-selective COX inhibitor, completely blocked the hyperventilation and blood gases changes induced by AA. In addition, central pretreatment with different doses of furegrelate, a TXA2 synthesis inhibitor, also partially prevented AA-evoked hyperventilation and blood gases effects. These data explicitly show that centrally administered AA induces hyperventilation with increasing pO2 and decreasing pCO2 levels which are mediated by the activation of central COX to TXA(2) signaling pathway.
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    Ficus carica latex prevents invasion through induction of let-7d expression in GBM cell lines
    (Springer, 2015-03) Bilir, Ayhan; Tezcan, Gülçin; Tunca, Berrin; Bekar, Ahmet; Yalçın, Murat; Şahin, Saliha; Budak, Ferah; Çeçener, Gülşah; Egeli, Ünal; Demir, Cevdet; Güvenç, Gökçen; Yılmaz, Gözde; Erkan, Leman Gizem; Malyer, Hulusi; Taşkapılıoğlu, Mevlüt Özgür; Evrensel, Türkkan; Uludağ Üniversitesi/Tıp Fakültesi/Biyoistatistik Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Beyin ve Sinir Cerrahisi Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Kimya Bölümü.; Uludağ Üniversitesi/Tıp Fakültesi/Mikrobiyoloji Anabilim Dalı.; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Biyoloji Bölümü.; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Onkoloji Anabilim Dalı.; 0000-0002-5956-8755; 0000-0002-1619-6680; 0000-0002-5600-8162; 0000-0003-2887-5688; 0000-0001-7625-9148; 0000-0002-3820-424X; 0000-0001-7904-883X; 0000-0002-9381-0410; 0000-0002-1413-3651; 0000-0002-6283-4540; 0000-0001-5472-9065; 0000-0002-9732-5340; AAH-3843-2020; ABI-6078-2020; CGB-7869-2022; AAG-6956-2021; AAH-2892-2021; F-4657-2014; AAP-9988-2020; AAH-1420-2021; DTQ-5753-2022; AAR-6815-2021; JFV-9885-2023; CNS-3398-2022; DDS-8738-2022; AAW-5254-2020; AAJ-1027-2021; 25650627600; 6602965754; 6603677218; 57192959734; 15027401600; 6701913697; 6508156530; 55665145000; 7003565902; 56529426800; 56529070300; 56529371200; 6602736554; 25936798300; 6603942124
    Glioblastoma multiforme (GBM) is one of the deadliest human malignancies. A cure for GBM remains elusive, and the overall survival time is less than 1 year. Thus, the development of more efficient therapeutic approaches for the treatment of these patients is required. Induction of tumor cell death by certain phytochemicals derived from medicinal herbs and dietary plants has become a new frontier for cancer therapy research. Although the cancer suppressive effect of Ficus carica (fig) latex (FCL) has been determined in a few cancer types, the effect of this latex on GBM tumors has not been investigated. Therefore, in the current study, the anti-proliferative activity of FCL and the effect of the FCL-temozolomide (TMZ) combination were tested in the T98G, U-138 MG, and U-87 MG GBM cell lines using the WST-1 assay. The mechanism of cell death was analyzed using Annexin-V/FITC and TUNEL assays, and the effect of FCL on invasion was tested using the chick chorioallantoic membrane assay. To determine the effect of FCL on GBM progression, the expression levels of 40 GBM associated miRNAs were analyzed in T98G cells using RT-qPCR. According to the obtained data, FCL causes cell death in GBM cells with different responses to TMZ, and this effect is synergistically increased in combination with TMZ. In addition, the current study is the first to demonstrate the effect of FCL on modulation of let-7d expression, which may be an important underlying mechanism of the anti-invasive effect of this extract.
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    Modulation of arachidonic acid-evoked cardiorespiratory effects by the central lipoxygenase pathway
    (Elsevier, 2020-07) Bayram, Gökçen Güvenç; Altınbaş, Burçin; Erkan, Leman Gizem ; Yalçın, Murat; Bursa Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0002-9534-736X; 0000-0002-5600-8162; IYS-2646-2023; AAR-6815-2021; AAG-6956-2021; CNS-3398-2022; 57216410828; 55356919300; 56529371200; 57192959734
    We previously reported that intracerebroventricularly (ICV) injected arachidonic acid (AA) could produce pressor and bradycardic responses on the cardiovascular system and hyperventilation effect on the respiratory system by activating cyclooxygenase (COX). We also demonstrated that centrally injected AA-induced cardiovascular and respiratory responses were mediated by COX-metabolites, such as thromboxane A(2) (TXA(2)), prostaglandin (PG) D, PGE, and PGF(2 alpha). Brain tissue is also able to express the lipoxygenase (LOX) enzyme and LOX-induced AA-metabolites. The current study was designed to investigate the possible mediation of the central LOX pathway in AA-induced cardiorespiratory effects in anesthetized rats.Central pretreatment with different doses of a non-selective LOX inhibitor, nordihydroguaiaretic acid (NDGA) (500 and 1000 mu g; ICV) partially blocked the AA (0.5 mu mol; ICV)-evoked pressor and bradycardic cardiovascular responses in male anesthetized Sprague Dawley rats. Pretreatment with different doses of NDGA (500 and 1000 mu g; ICV) also reduced AA-induced hyperventilation responses, with an increase in tidal volume, respiratory rate and minute ventilation, in the rats. Moreover, AA-induced increasing pO(2) and decreasing pCO(2) responses were diminished by central NDGA pretreatment.In summary, our findings show that the central LOX pathway might mediate, at least in part, centrally administered AA-evoked cardiorespiratory and blood gases responses.
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    The role of centrally injected nesfatin-1 on cardiovascular regulation in normotensive and hypotensive rats
    (Elsevier, 2015-12) Yılmaz, Mustafa Sertaç; Altınbaş, Burçin; Güvenç, Gökçen; Erkan, Leman Gizem; Avşar, Özge; Savcı, Vahide; Küçükşen, Duygu Udum; Arıcan, İlker; Yalçın, Murat; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Veterinerlik Fakültesi/Fizyoloji Anabilim Dalı.; Uludağ Üniversitesi/Veterinerlik Fakültesi/Biyokimya Anabilim Dalı.; Uludağ Üniversitesi/Veterinerlik Fakültesi/Anatomi Anabilim Dalı.; 0000-0001-9496-1475; 0000-0002-9534-736X; 0000-0002-1413-3651; 0000-0001-7052-1694; 0000-0001-6342-0094; 0000-0002-5600-8162; AAH-1571-2021; AAR-6815-2021; AAH-5167-2021; AAG-7518-2021; AAG-6956-2021; 8895544100; 55356919300; 56529426800; 56529371200; 56764150800; 6603687024; 56764576200; 14055524200; 57192959734
    This study investigated the cardiovascular effects of nesfatin-1 in normotensive rats and animals subjected to hypotensive hemorrhage. Hemorrhagic hypotension was induced by withdrawal 2 mL blood/100 g body weight over a period of 10 min. Acute hemorrhage led to a severe and long-lasting decrease in mean arterial pressure (MAP) and heart rate (HR). Intracerebroventricularly (i.c.v.) administered nesfatin-1 (100 pmol) increased MAP in both normotensive and hemorrhaged rats. Nesfatin-1 also caused bradycardia in normotensive and tachycardia in hemorrhaged rats. Centrally injected nesfatin-1 (100 pmol, i.c.v.) also increased plasma catecholamine, vasopressin and renin concentrations in control animals and potentiated the rise in all three cardiovascular mediators produced by hemorrhage. These findings indicate that centrally administered nesfatin-1 causes a pressor response in conscious normotensive and hemorrhaged rats and suggest that enhanced sympathetic activity and elevated vasopressin and renin concentrations mediate the cardiovascular effects of the peptide.
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    Screening of cytotoxic, anti-angiogenic, anti-tumorogenic and antimicrobial activities of Anatolian Vipera ammodytes (Nose-horned viper) venom
    (Walter de Gruyter Gmbh, 2016-05-31) İğci, Naşit; Nalbantsoy, Ayşe; Yalçın, Hüsniye Tansel; Göçmen, Bayram; Erkan, Leman Gizem; Akça, Gözde Yılmaz; Yalçın, Murat; Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; 0000-0002-5600-8162; AAG-6956-2021; 56529371200; 57203599081; 57192959734
    Objective: In the present study, we aimed to screen the cytotoxic, antimicrobial, anti-angiogenic and anti-tumorogenic activities of Anatolian Vipera ammodytes (Nose-horned Viper) crude venom. Material and methods: The cytotoxicity was screened against PC3, HeLa, CaCo-2, U-87MG, MCF-7 and Vero cells by using MTT assay. The antimicrobial activity on Escherichia coli ATCC 25922, E. coli 0157: H7, Enterococcus faecalis 29212, Enterococcus faecium DSM 13590, Staphylococcus aureus ATCC 25923, Staphylococcus epidermidis ATCC 12228, Salmonella typhimirium CCM 5445, Proteus vulgaris ATCC 6957, Bacillus cereus ATCC 7064 and Candida albicans ATCC 10239 was assayed by determining the minimum inhibitory concentration using the broth dilution method. Anti-angiogenic and anti-tumorogenic activity was assessed by using chick chorioallantoic membrane (CAM) assay. Results: The IC50 value of V. ammodytes venom on cultured cells varied from 1.8 to 7.0 mu g/mL after 48 h treatment. Venom showed antimicrobial activity on P. vulgaris, S. aureus, S. epidermidis, E. faecium and C. albicans (the highest activity). The venom exhibited dose-dependent anti-angiogenic activity on CAM model at 2 and 10 mu g/mL doses with scores of 1.1 and 2.0, respectively. Conclusion: The results of the present study contributed to the knowledge of the biological activities of Anatolian V. ammodytes venom and showed its potential for further bioactivity guided characterization studies.
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    Serebral yan ventriküle enjekte edilen araşidonik asitin solunum sistemine etkisi: Etkiye aracılık eden merkezi mekanizmaların araştırılması
    (Uludağ Üniversitesi, 2016-05-25) Erkan, Leman Gizem; Yalçın, Murat; Uludağ Üniversitesi/Sağlık Bilimleri Enstitüsü/Veteriner Fizyoloji Anabilim Dalı.
    Bu çalışmada merkezi yolla uygulanan araşidonik asitin (AA) solunum düzenlenmesinde ve kan gazlarına etkilerini belirlemek ve bu etkilerde merkezi siklooksijenaz (COX), lipooksijenaz (LOX), tromboksan A2 (TXA2), prostagladin (PG) E ve D'nin aracılığının belirlenmesi amaçlanmıştır. Yapılan çalışmada Spraque Dawley ırkı (250-300 g) 140 tane erişkin erkek sıçanlar kullanıldı. Sıçanlar ketamin (50 mg/kg; i.m.) ksilazin (20 mg/kg; i.m.) karışımı ile anestezi edildi. Anestezi altında, solunum parametrelerinin takip edilebilmesi için tüm hayvanlara trekeostomi yapıldı. Kan gazı parametrelerinin incelenmesi için gerekli kan örneklerinin toplanabilmesi amacıyla sıçanların sol femoral arterlerine ise heparin içeren % 0,9 tuzlu su (50 Ü/ml) ile doldurulmuş polietilen kateter (PE 50), yerleştirildi. Merkezi yolla ilaç enjeksiyonları için serebral yan ventriküle (s.y.v) 22 G paslanmaz çelik iğneden hazırlanmış klavuz kanül yerleştirildi. Çalışmada ilk olarak merkezi yolla uygulanan AA'nın solunum parametreleri yani; tidal volüm (TD), solunum sayısı (SS), dakika solunum hacmi (DSH), üzerine etkileri ve kan gazları; parsiyel oksijen (pO2) ve parsiyel karbondioksit (pCO2) basınçları üzerine değişimler araştırıldı. AA (0,25, 0,5 ve 1 µmol; s.y.v.) doza- ve zamana- bağlı olarak sıçanlarda tüm solunum parametreleri ve pO2 de artışa neden olup pCO2 de düşüşe neden olmuştur. AA'nın oluşturduğu bu etkilerde merkezi COX, LOX, TXA2, PGE2 ve PGD2' nin aracılığını göstermek için seçici olmayan COX inhibitörü ibuprofen (250 µg; s.y.v.), seçici olmayan LOX inhibitörü nordihydroguaiaretic asit (NDGA) (500 µg; s.y.v.), TXA2 sentez inhibitörü furegrelate (250 µg; s.y.v.) veya PGE ve PGD reseptör antagonisti AH6809 (10 µg; s.y.v.) ön tedavisi, AA (0,5 µmol; s.y.v.) tedavisinden 10 dakika önce uygulandı. İbuprofen tamamen, NDGA, furegrelate ve AH6809 ise kısmen AA'nın oluşturduğu solunum parametreleri ve kan gazı etkilerini bloke etti. Sonuç olarak, elde ettiğimiz sonuçlar merkezi olarak uygulanan AA'nın sıçanlarda hiperventilasyona yol açtığı, ve AA'nın solunum parametreleri etkilerinde merkezi COX-TXA2 –PGE2 ve PGD2 yolağı ve ayrıca LOX yolağı kısmen aracılık etmektedir.
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    The effect of centrally injected arachidonic acid on respiratory system
    (Wiley, 2015-09-01) Erkan, Leman Gizem; Güvenç, Gökçen; Altınbaş, Burçin; Yalçın, Murat; Erkan, Leman Gizem; Güvenç, Gökçen; Altınbaş, Burçin; YALÇIN, MURAT; Uludağ Üniversitesi/Veteriner Fakültesi; 0000-0002-1413-3651; 0000-0002-5600-8162; 0000-0002-9534-736X; IYS-2646-2023; AAR-6815-2021; AAG-6956-2021; CNS-3398-2022
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    The effect of histamine on acetylcholine and choline releases from the posterior hypothalamus and nucleus tractus solitarius of hypotensive rats
    (Wiley, 2015-09-01) Altınbaş, Burçin; Güvenç, Göken; Erkan, Leman Gizem; Yılmaz, Mustafa Sertaç; Avşar, Özge Avşar; Yalçın, Murat Yalçın; Altınbaş, Burçin; Güvenç, Göken; Erkan, Leman Gizem; YILMAZ, MUSTAFA SERTAÇ; Avşar, Özge Avşar; YALÇIN, MURAT; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Bölümü; 0000-0001-9496-1475; 0000-0002-5600-8162; 0000-0002-9534-736X; AAG-6956-2021; IYS-2646-2023; AAH-1571-2021; CTA-3293-2022; CNS-3398-2022; CCB-6768-2022
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    The investigation of the mediation cyclooxygenase-tromboxane A2 pathways in centrally injected orexin-induced cardiovascular effect
    (Wiley, 2015-09-01) Güvenç, Gökçen; Erkan, Leman Gizem; Altınbaş, Burçin; Aydın, Begüm; Yalçın, Murat; Güvenç, Gökçen; Erkan, Leman Gizem; Altınbaş, Burçin; Aydın, Begüm; YALÇIN, MURAT; Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Kimya Bölümü.; 0000-0002-5600-8162; AAG-6956-2021; IYS-2646-2023; FCF-0163-2022; CNS-3398-2022; HLA-3520-2023