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Öğe Age- and Sex- Dependent Changes in Serum Levels of TAS, TOS, TLR2, TLR4, HSP60, HSP90, and HMGB1(Duzce Univ, Fac Medicine, 2023) Kaya, Salih TuncObjective: Cellular and physiological functions may be affected in an age-and sex-specific manner. The aim of this study is to investigate sex-and age-specific differences in the serum levels of Total Antioxidant Status (TAS), Total Oxidant Status (TOS), Oxidative Stress Index (OSI), Toll-Like Receptor 2 (TLR2), Toll-Like Receptor 4 (TLR4), Heat Shock Protein 60 (HSP60), Heat Shock Protein 90 (HSP90), and High Mobility Group Box 1 (HMGB1) as well as to examine the correlation between them.Method: Four groups of mice, each including seven animals, were used in the present study: young males and females (6 months old); old males and females (24 months old). Blood samples were taken from the heart and serum was used to assay the levels of TLR2, TLR4, HSP60, HSP90, HMGB1, TAS and TOS.Results: HGMB1, TOS and OSI were higher in old females than in young females (p<0.05). TLR2 and TLR4 levels were higher in young females than in young males; however, HSP60 was lower in young females than in young males (p<0.01). HSP60 was lower in old males than in young males (p<0.05). Positive correlations were present between TLR2, TLR4 and HMGB1 (p=0.001, r=0.096; p=0.012, r=0.867; p=0.002, r=0.935, respectively) as well as between HMGB1 and HSP60 (p=0.049, r=0.756) in young females. A negative correlation was detected between HSP90 and TLR4 in young males (p=0.000, r=-0.982), and between HSP60 and TLR2, OSI in old males (p=0.014, r=-0.856; p=0.042, r=-0.772, respectively).Conclusion: The results of present study indicated that age and sex may be important factors for serum levels of TLR2, TLR4, HSP60, HSP90, HMGB1 and OSI as well as the correlation between them.Öğe Decreasing myocardial estrogen receptors and antioxidant activity may be responsible for increasing ischemia- and reperfusion-induced ventricular arrhythmia in older female rats(Pergamon-Elsevier Science Ltd, 2021) Bozdogan, Omer; Bozcaarmutlu, Azra; Kaya, Salih Tunc; Sapmaz, Canan; Ozarslan, Talat Ogulcan; Eksioglu, Didem; Yasar, SelcukAims: This study aimed to investigate the relationship between ischemia- and reperfusion-induced arrhythmia and blood serum estrogen levels, myocardial estrogen receptor levels, antioxidant enzyme activities, and the effects of the estrogen receptor blocker, fulvestrant (ICI 182 780). Main methods: A total of 102 female Sprague-Dawley rats of different ages (2-3, 6-7, 14-15, and 20-21 months) were used in this study. Myocardial ischemia was produced by ligation of the descending branch of the left anterior descending coronary artery, and reperfusion was produced by releasing this artery. An electrocardiogram (ECG) and blood pressure were recorded for 6 min of ischemia and 6 min of reperfusion. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), estrogen receptor alpha (ER alpha), and estrogen receptor beta (ER beta) in myocardial tissue and 17 beta-estradiol (E2) in blood serum were measured via enzyme-linked immunosorbent assay (ELISA). The results were compared using a Mann-Whitney U test, one-way analysis of variance (ANOVA), and a student's t-test. Key findings: It is not the changes in serum estrogen levels but the decreasing myocardial estrogen receptors and antioxidant activities that could be responsible for the occurrence of more severe arrhythmia in response to reperfusion in older female rats. Significance: The death rate due to a heart attack in younger men is higher than in women. However, it equalizes after the menopausal stage in women. In this study, the reason for the increasing sudden post-menopausal death rate in women was investigated experimentally.Öğe Diazoxide attenuates DOX-induced cardiotoxicity in cultured rat myocytes(Taylor & Francis Ltd, 2024) Guven, Celal; Taskin, Eylem; Aydin, Ozgul; Kaya, Salih Tunc; Sevgiler, YusufDoxorubicin (DOX)-induced cardiotoxicity is a well known clinical problem, and many investigations have been made of its possible amelioration. We have investigated whether diazoxide (DIA), an agonist at mitochondrial ATP-sensitive potassium channels (mitoKATP), could reverse DOX-induced apoptotic myocardial cell loss, in cultured rat cardiomyocytes. The role of certain proteins in this pathway was also studied. The rat cardiomyocyte cell line (H9c2) was treated with DOX, and also co-treated with DOX and DIA, for 24 h. Distribution of actin filaments, mitochondrial membrane potential, superoxide dismutase (SOD) activity, total oxidant and antioxidant status (TOS and TAS, respectively), and some protein expressions, were assessed. DOX significantly decreased SOD activity, increased ERK1/2 protein levels, and depolarised the mitochondrial membrane, while DIA co-treatment inhibited such changes. DIA co-treatment ameliorated DOX-induced cytoskeletal changes via F-actin distribution and mitoKATP structure. Co-treatment also decreased ERK1/2 and cytochrome c protein levels. Cardiomyocyte loss due to oxidative stress-mediated apoptosis is a key event in DOX-induced cytotoxicity. DIA had protective effects on DOX-induced cardiotoxicity, via mitoKATP integrity, especially with elevated SUR2A levels; but also by a cascade including SOD/AMPK/ERK1/2. Therefore, DIA may be considered a candidate agent for protecting cardiomyocytes against DOX chemotherapy.Öğe The effect of co-administration of berberine, resveratrol, and glibenclamide on xenobiotic metabolizing enzyme activities in diabetic rat liver(Taylor & Francis Ltd, 2020) Bozcaarmutlu, Azra; Sapmaz, Canan; Bozdogan, Omer; Kukner, Aysel; Kilinc, Leyla; Kaya, Salih Tunc; Eksioglu, DidemIt is possible to use plant-derived antioxidant molecules in the form of dietary supplements. However, dietary supplement-drug interaction pattern has not been well defined for most of these products. The aim of this study was to determine the effects of berberine, resveratrol, and glibenclamide on xenobiotic metabolizing enzyme activities in diabetic rats. Streptozotocin was administered to create experimental diabetes. Resveratrol (5 mg/kg) (R), glibenclamide (5 mg/kg) (G), and berberine (10 mg/kg) (B) were administered individually or in combinations in DMSO by intraperitoneal administration route to the diabetic rats. DMSO was also given to non-diabetic control (C) and diabetic control (D) groups. Livers of rats were taken under anesthesia at the end of the treatment period (12 days). Ethoxyresorufin O-deethylase (EROD), pentoxyresorufin O-depentylase (PROD), aniline 4-hydroxylase (A4H), erythromycin N-demethylase (ERND), glutathione S-transferase (GST), catalase (CAT), and glutathione reductase (GR) activities were measured in microsomes and cytosols. In addition, histomorphological studies were also performed in the liver tissues. EROD activity of D+R was significantly higher than C and D+R+B. PROD activity of D+R was significantly higher than C, D, D+R+G, D+R+B, and D+R+B+ G. PROD activity of D+B was significantly higher than C and D+R+B. ERND activity of D+R was significantly higher than D+R+G and D+R+B. GST activity of D+R was significantly higher than D+R+G. CAT activity of D+B was significantly lower than C. It is clear that co-administration of resveratrol, berberine, and glibenclamide modifies some of the important xenobiotic metabolizing enzyme activities. Resveratrol and berberine have the potential to cause dietary supplement-drug interaction.Öğe An Evaluation of Damages Caused by Doxorubicin in Liver Tissue and Potential Protective Effect of Propolis on These Damages(Duzce Univ, Fac Medicine, 2022) Orak, Nursen; Arslan, Gulgun Cakmak; Kaya, Salih TuncObjective: Doxorubicin (DOX), one of the chemotherapeutic drugs utilized in cancer treatment, has limited clinical use due to its serious toxic effects on non-target organs. The purpose of this study is to reveal the harmful effects of DOX in rat liver and the possible protective effect of propolis (PRPLS), a mixture of various herbal products collected by honeybees, on these damages by Attenuated Total Reflection-Fourier Transformation Infrared (ATR-FTIR) spectroscopy. Methods: Sprague dawley rats were separated into 4 groups; control, DOX (cumulative dose: 15 mg/kg), PRPLS (200 mg/kg) and DOX + PRPLS. The rats were given 200 mg/kg PRPLS by oral gavage daily for 20 consecutive days and 2.5 mg/kg DOX intraperitoneally on days 10, 12, 14, 16, 18 and 20 of the experiment. 24 hrs after the last administrations, liver samples were collected and examined by ATR-FTIR spectroscopy. Results: DOX caused a decrease in the amount of glycogen and nucleic acids, an increase in the amount of lipids and proteins and some important changes in the metabolism, structure and conformation of these molecules in the liver. DOX also induced lipid peroxidation, an increase in membrane fluidity, a decrease in membrane order and protein denaturation. PRPLS did not induce any toxic effect on the liver when it was given alone and PRPLS administered before DOX was not effective to eliminate these harmful effects of DOX. Conclusions: DOX caused significant structural and compositional changes in liver tissue and PRPLS was inadequate to prevent these changes at the dose and time used here.Öğe Investigation of genotoxic effects of rhododendron honey using three mammalian bioassays in vivo(Taylor & Francis Ltd, 2021) Rasgele, Pinar Goc; Gokalp, Fulya Dilek; Kaya, Salih Tunc; Kekecoglu, Meral; Acar, Merve KamburRhododendron honey (RH) is obtained from the rhododendron plants are grown in many regions around the world, causes poisoning in humans due to the grayanotoxin (GTX) compound in its structure. It is used by the public as a therapeutic for some diseases. It was aimed to study the genotoxic and cytotoxic effects of RH in mouse bone-marrow and sperm cells by using three mammalian bioassays. 25, 50 and 75 mg kg(-1) concentrations of RH given to male mice via gavage for 24 and 48 h treatment periods and its active ingredient Grayanatoxin (GTX-III) 0.01 mg kg(-1) by i.p. injection. Chromosome aberrations (CA), polychromatic erythrocytes (PCE)/normochromatic erythrocytes (NCE), micronucleated polychromatic erythrocytes (MNPCE) and sperm abnormalities were investigated. The results demonstrated that all the tested concentrations of RH significantly induced total abnormal cell frequency including chromosomal breaks for two time periods. In the MN assay, 75 mg kg(-1) RH and 0.01 mg kg(-1) GTX-III significantly increased % MNPCE and significantly reduced PCE/NCE ratios after 24 and 48 h treatments on mice demonstrating potential genotoxic and cytotoxic effect. Although there was a concentration-related increase in the percentage of total sperm abnormalities, this increase was not statistically significant compared to control. As a result, microscopic genotoxicity and cytotoxicity marker tests showed that RH and its active ingredient GTX-III have potential genotoxic and cytotoxic effect on mice bone marrow cells. It is understood that RH that is used to treat some diseases by public, should be handled carefully and used in a controlled manner.Öğe Myocardial Infarction in Diabetes and Its Relationship with KATP Channels(Wiley, 2023) Kaya, Salih Tunc[No abstract available]Öğe Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction(Imprimatur Publications, 2020) Taskin, Eylem; Guven, Celal; Kaya, Salih Tunc; Sariman, Melda; Emrence, Zeliha; Ekmekci, Sema Sirma; Akcakaya, 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.
