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Öğe Diyabette Leptin Hormonun Olası Etkileri(2019) Taşkın, Eylem; Güven, Celal; Kaya, Salih Tunç; Sevgiler, YusufŞeker hastalığı olarak bilinen diyabet, çeşitli komplikasyonları (kalp ve dolaşım hastalıkları, kanser ve buna benzerhastalıklar) beraberinde getiren, insan hayatını olumsuz yönde etkileyen metabolik bir hastalıktır. Genel olarakdiyabet tip I ve tip II olmak üzere iki büyük alt grupta toplanan bir hastalıktır. Tip I diyabette beta (?) hücrelerininapoptoz ile kaybı insülin salgısının azalmasında önemli bir mekanizmadır. Leptin de insülin gibi antiapoptotik veproliferatif hormonlardan biridir. Dahası düşük leptin ve insülin tedavisinin sadece yüksek doz insülin kullanımınaoranla kan şekerinin tamponlanmasında daha etkili olduğu bildirilmektedir. Fakat leptinin tip I diyabetteki buetkisi/etkileri hala gizemini korumaktadır. Leptinin tip I diyabetteki önemli etkisinden biri de yağların ?oksidasyonunun artmasına neden olarak, kan şekerinin tamponlanmasını da sağları. Bu da insülin direncininoluşmasının azalmasına neden olmaktadır. Ayrıca leptinin insülinin anabolik etkilerini taklit ettiği gibi diyabettemeydana gelen ketoasidozu önlediği de vurgulanmaktadır. Dolayısıyla leptin tedavisi, zorunlu yüksek doz insülinkullanımı azaltılmasına olanak tanıyabilmektedir. Bu derleme, literatürdeki leptin ve diyabet arasındaki bukarmaşık ilişkinin mekanizmasının aydınlatılmasında önemli bir katkı sağlayabilecek potansiyele sahiptir.Öğe Herbal medicine in diabetes mellitus with cardiovascular diseases(Springer International Publishing, 2019) Kaya, Salih Tunç; Güven, Celal; Taşkın, Eylem[No abstract available]Öğe HMGB1: Functions, inhibitors and clinical significance(Nova Science Publishers, Inc., 2022) Taşkın, E.; Güven, Celal; Kaya, Salih TunçDamage-associated molecular patterns (DAMPs), a term also known as alarmins coined by Walter G. Land, Seong, and Matzinger, are endogenous danger molecules that are released from damaged or dying cells and activate the innate immune system by interacting with pattern recognition receptors (PRRs). One of the most well-known DAMPs is High Mobility Group Box-1 (HMGB1), the name being such due to its very fast movement in gel electrophoresis. Importantly, HMGB1 has been shown to contribute to the pathogenesis of various diseases including myocardial ischemia/reperfusion injury, epilepsy, diabetes, multiple sclerosis, cancer, as well as hepatic steatosis, and fatty liver disease. There are three sections in the book. The first section is named HMGB1 and Cancer, including two chapters. One of the chapters is focused on HMGB1 in cancer therapy and managing COVID-19 infection, as well as multiple sclerosis. The second chapter in the first section is the crosstalk between cancer and myocardial ischemia/reperfusion injury (MIR) through HMGB1 via ferroptotic cell death. The second section is HMGB1 and metabolic interactions, consisting of two chapters. The first chapter is HMGB1 and inflammation in adipose tissue, resulting in insulin resistance and type 2 diabetes. The second chapter in the second section sums up recent data related to HMGB1 and liver injury, e.g., drug-induced liver injury, alcoholic liver disease, non-alcoholic fatty liver disease, viral hepatitis, sepsis, and acute chronic liver failure, hepatocellular death through oxidative stress, inflammatory signaling, and autophagy in hepatocytes. The third section is about HMGB1 and neurodegenerative diseases. The section contains four chapters. The first chapter in the section evaluates HMGB1 and its antagonist in brain disorders, including epilepsy, headache, neuroimmunological disorders, neurodegenerative disorders, and stroke. The second chapter in the third section is about the role of HMGB1 on post-brain injury, including potential mechanisms and therapeutic opportunities as well. The third chapter in the third section evaluates the interaction of HMGB1 and Multiple sclerosis via TLR4/NF-?B signaling pathway, leading to the release of proinflammatory cytokines causing an inflammatory response. The last chapter aims to explain the effects of HMGB1 on epilepsy. © 2023 by Nova Science Publishers, Inc. All rights reserved.Öğe HMGB1’in Kanser ve Tedavisiyle İlişkisi(2019) Taşkın, Eylem; Güven, Celal; Kaya, Salih Tunç; Sevgiler, YusufYüksek mobilite grup kutusu 1 (HMGB1) histon olmayan DNA proteini olup, kısaca DAMP olarak ifade edilen(Damage-associated molecular pattern) tehlike sinyali veya alarmı olarak görev yapar. Hasarlanmış veya kanserlihücrelerden salınan HMGB1, gelişmiş glikasyon son ürünleri için reseptör (RAGE) ve Toll benzeri reseptörlerine(TLRs) bağlanarak mitojenle aktive olan kinaz (MAPK)’ları aktive ederek hücre içi etkilerini oluşturur. HMGB1kanser ilaçlarına karşı gelişen dirençte önemli rol oynar. Aynı zamanda, yumuşak doku kanserlerine karşıkullanılan ilaçlardan biri olan adriyamisinin (ADR) neden olduğu kalp yetmezliğinin gelişiminde de önemli roloynağına dair kanıtlar mevcuttur. Dolayısıyla HMGB1 kanser tedavisinde ilaçlara karşı gelişen direncin ve/veyailacın toksik etkisine karşı iyi bir terapötik ajan adayıdır. Bu derlemenin amacı, HMGB1 ile kanser ve tedavisindekullanılan bir ilaç olan ADR arasındaki ilişkiyi açıklamaktır.Öğe The Identification of Intracellular Signalling Pathway Through DHMGB1/TLR2 Axis on Myocardial Ischemia/Reperfusion Injury-Induced Apoptosis(Wiley, 2022) Güven, Eylem Taşkın; Güven, Celal; Kaya, Salih Tunç; Keles, Ayse Ikinci; Destegul, Dilek; Pelit, Aykut; Günay, İsmail[Bastract Not Available]Öğe Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia(Int Scientific Literature, Inc, 2016) Taşkın, Eylem; Tuncer, Kadir Ali; Güven, Celal; Kaya, Salih Tunç; Dursun, NurcanBackground: Myocardial ischemia and reperfusion lead to impairment of electrolyte balance and, eventually, lethal arrhythmias. The aim of this study was to investigate the effects of pharmacological inhibition of angiotensin-II (Ang-II) production on heart tissue with ischemia-reperfusion damage, arrhythmia, and oxidative stress. Material/Methods: Rats were divided into 4 groups: only ischemia/reperfusion (MI/R), captopril (CAP), aliskiren (AL), and CAP+AL. The drugs were given by gavage 30 min before anesthesia. Blood pressure and electrocardiography (ECG) were recorded during MI/R procedures. The heart tissue and plasma was kept so as to evaluate the total oxidant (TOS), antioxidant status (TAS), and creatine kinase-MB (CK-MB). Results: Creatine kinase-MB was not different among the groups. Although TAS was not affected by inhibition of Ang-II production, TOS was significantly lower in the CAP and/or AL groups than in the MI/R group. Furthermore, oxidative stress index was significantly attenuated in the CAP and/or AL groups. Captopril significantly increased the duration of VT during ischemia; however, it did not have any effect on the incidence of arrhythmias. During reperfusion periods, aliskiren and its combinations with captopril significantly reduced the incidence of other types of arrhythmias. Captopril alone had no effect on the incidence of arrhythmias, but significantly increased arrhythmias score and durations of arrhythmias during reperfusion. MAP and heart rate did not show changes in any groups during ischemic and reperfusion periods. Conclusions: Angiotensin-II production appears to be associated with elevated levels of reactive oxygen species, but Ang-II inhibitions increases arrhythmia, mainly by initiating ventricular ectopic beats.Öğe The role of ferroptotic cell death-related HMGB1 in inflammation crosstalk with cancer and myocardial Ischemia/reperfusion injury(Nova Science Publishers, Inc., 2022) Kaya, Salih Tunç; Güven, Celal; Taşkın, E.Inflammation is one of the critical defense pathways against pathogen and pathologic conditions, including cancer and myocardial ischemia/ reperfusion (MIR) injury. Therefore, inflammation has positive and negative impacts on tissues and organs. There are two types of inflammation, named as acute and chronic inflammation. The inflammation is also involved in the development of cancer and myocardial infarction. Damage-associated molecular patterns (DAMPs), such as High Mobility Group Box-1 (HMGB1), heat shock proteins (HSPs), ATP, and S100 proteins, are conservative danger molecules released from damaged or dying cells to trigger an immune response. However, they have essential roles in pathological inflammation to participate in self-defense in physiological and pathological circumstances. Recent evidence has emerged that inflammation may be a significant factor in the development and/or progression of cancer and myocardial infarction. Herein, we review current research on the role of HMGB1 in cancer and myocardial ischemia/reperfusion injury, focusing on inflammation. Furthermore, we have discussed the role of the posttranslational modification of HMGB1 in both illnesses. In addition, we focus on a new cell death pathway named ferroptosis, which may be involved in the development of both cancer and MIR through inflammation by HMGB1. © 2023 by Nova Science Publishers, Inc. All rights reserved.Öğe The role of toll-like receptors in the protective effect of melatonin against doxorubicin-induced pancreatic beta cell toxicity(Pergamon-Elsevier Science Ltd, 2019) Taşkın, Eylem; Güven, Celal; Kaya, Salih Tunç; Şahin, Leyla; Kocahan, Sayad; Değirmencioğlu, Arife Zuhal; Sevgiler, YusufAims: Doxorubicin, an anticancer drug, has a toxic effect on many tissues such as heart, pancreas, liver, kidney, and testis. The aim of current study is to investigate whether melatonin would be protective in doxorubicin-induced beta (beta) cell toxicity via HMGB1/TLR2/TLR4/MAPK/NF-kappa B signaling pathway. Main methods: Human pancreatic beta cell (1.1B4) was used in the present study. Four experimental groups were created as control, melatonin (10 mu M), doxorubicin (2 mu M) and the combination of melatonin with doxorubicin. Following 24-h treatment, Mitogen-activated protein kinase (MAPKs), Toll like receptors (TLRs) including TLR2 and TLR4, pro-and anti-apoptotic protein expression levels were determined by western blotting. Total antioxidant (TAS), oxidant status (TOS) and oxidative stress index (OSI) of the cells as well as superoxide dismutase (SOD) levels were determined. Active caspase-8 activity was measured and TUNEL staining was performed to study apoptotic pathways. Mitochondrial membrane potential (MMP), some protein expressions and F-actin distribution were analyzed. Key findings: Doxorubicin caused to depolarize MMP, resulting in enhancing apoptosis by activation of caspase-8 via MAPKs/NF-kappa B pathway via elevation of TOS and decreasing TAS. Also, doxorubicin destroyed F-actin distribution and elevated TLR2 and some apoptotic proteins, including Bax. However, co-treatment of melatonin with doxorubicin could reverse depolarization of MMP and inhibition of apoptosis through MAPK/NF-kappa B signaling by decreasing TOS and increasing TAS. The co-treatment reversed the alternations of TLR2, TLR4, MAPKs and apoptotic protein expressions induced by doxorubicin. Significance: Melatonin could be a good candidate against pancreatic beta cell toxicity-induced by doxorubicin through TLR2/TLR4/MAPK/NF-kappa B pathways.Öğe Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction(Imprimatur Publications, 2020) Taşkın, Eylem; Güven, Celal; Kaya, Salih Tunç; Sarıman, Melda; Emrence, Zeliha; Ekmekci, Sema Sırma; Akçakaya, HandanPurpose: Adriamycin (APR) is a commonly used anti-cancer drug. ADR has toxic effects on cardiomyocytes and leads to heart failure. However, the underlying mechanism(s) by which ADR causes heart failure is still not clarified exactly. The aim of present study is to investigate whether ADR-induced heart failure is mediated via HMGB1/TLR4 to initiate the apoptosis through MAPK/AMPK pathways. Methods: H9c2 cell line was used to create four groups as a control, HMGB1 inhibition, ADR, ADR+HMGB1 inhibition. Silencing HMGB1 was performed with specific small interfering RNA. ADR was used at 2 mu M concentration for 36 and 48 hours. Protein and genes expressions, apoptosis was measured. Results: Although ADR decreased AMPK, pAMPK, ERK1/2, pERK1/2, p38, JNK protein expression, ADR+HMGB1 inhibition led to change those protein expressions. The effect of silencing of HMGB1 prevented apoptosis induced by ADR in the cells. HMGB1 caused changes a kind of posttranscriptional modification on the TLR4 receptor. This posttranscriptional modification of TLR4 receptor led to decreased AMPK protein level, but phosphorylated-AMPK. This alternation of AMPK protein caused enhancing of JNK protein, resulting from the decline of p38 and ERK protein levels. Eventually, JNK triggered apoptosis by a caspase-dependent pathway. The number of TUNEL positive and active caspase 8 cells at ADR was high, although HMGB1 silencing could decrease the cell numbers. Conclusions: Inhibition of HMGB1 might prevent the lose of the cardiac cell by inhibition of apoptotic pathway, therefore HMGB1 plays an essential role as amplifying on ADR toxicity on the heart by TLR4.
