Person: BAHAR, ASLI NUR
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BAHAR
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ASLI NUR
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Publication Metadata only Protective effect of sirtuin 2 inhibition in D-Galactose-Induced renal aging and fibrosis(2023-12-04) BAHAR, ASLI NUR; Bahar A. N., Keskin Aktan A., Sonugür F. G., Akarca Dizakar S. Ö., Akbulut K. G.Publication Metadata only AGK-2 protects the tymus aganist D-Galactose induced senescense in rats(2023-12-04) BAHAR, ASLI NUR; Bahar A. N., Kavak H. K., Keskin Aktan A., Coşkun A., Akarca Dizakar S. Ö., Akbulut K. G.INTRODUCTION-AIM: Immune aging with advancing age is associated with thymic involution, changes in B and T cellnumbers, increased oxidative stress and apoptosis, and decreased autophagy. D-Galactose (D-Gal) administration is a modelused in aging. SIRT2, a member of the sirtuin family, has been shown to increase with age and inhibit autophagy. In this study,we aimed to investigate the effects of AGK2, a SIRT2 inhibitor, on malondialdehyde (MDA) for oxidative stress, SIRT2expression, LC3 as autophagy parameter, apoptosis parameters Bax, Bcl2, Bax/Bcl2 ratio and thymic histological structure inthymus tissue.METHODS: A total of 24 young male (3 months old) Sprague Dawley rats were used. Rats were divided into 4 groups asControl, D-Gal, Solvent+D- Gal L, D-Gal +AGK2+Solvent. D-galactose (150 mg/kg/day), AGK-2 (10μM/bw) as specific SIRT2inhibitor, 4% DMSO+PBS as solvent and saline were administered subcutaneously to the experimental and control groups for10 weeks. MDA level in thymus tissue was measured by spectrophotometer, SIRT2, apoptosis and autophagy related proteinlevels were measured by western blot method. Thymus structure was evaluated by HE staining. Statistical analysis wasperformed by ANOVA (post hoc LSD) and Pearson correlation test (p<0.05). Data were presented as mean±SEM.RESULTS: D-galactose administration increased MDA levels and decreased LC3 protein expression in thymus tissue. D-Galadministration caused thymus atrophy and loss of cortico-medullary border. AGK-2 treatment decreased MDA level, Baxexpression, Bax/Bcl-2 ratio, significantly increased LC3 level and restored cortex-medulla border and cell structure in thymustissue. LC3 was positively correlated with Bcl-2 and negatively correlated with Bax and Bax/Bcl2 ratio.CONCLUSION: Our study showed that AGK-2 decreased lipid peroxidation, induced autophagy and suppressed apoptosis inD-Galactose-induced aging, and may protect the thymus from the negative effects of aging.ACKNOWLEDGEMENT: This work was supported by Gazi University Scientific Research Project Foundation (Project No: TTU-2021-7192)Publication Open Access Signaling pathways in liver fibrosis(2023-01-01) BAHAR, ASLI NUR; BAHAR A. N., AKBULUT K. G.Liver fibrosis is a disease characterized by activation of hepatic stellate cells (HSCs) and excessive accumulation of extracellular matrix (ECM) components that destroy the physiological structure of the liver. Liver fibrosis contributes to the increasing prevalence and severity of chronic liver diseases. If liver fibrosis, which is of great clinical importance, is not treated, it ends with cirrhosis, which is characterized by fatal and intense complications. Cirrhosis can progress to hepatocellular carcinoma. Although fibrosis was previously thought to be an irreversible process, studies have shown that because of the liver\"s high regenerative ability, regression and return to normal architecture is higher than in other tissues, even in advanced disease.Targeting signaling pathways that cause fibrosis and anti-fibrotic therapies are needed to prevent the progression of liver disease and the development of hepatocellular carcinoma (HCC). Activation of HSCs and transforming growth factor beta (TGF-beta), Wnt/beta-catenin signaling pathways and interactions play an important role in the pathogenesis of the disease. Sirtuins (SIRT) belong to the sirtuin family of Nicotinamide Adenine Dinucleotide, (NAD+) dependent protein deacetylases and are involved in many important cellular biological processes, including the inflammatory response, oxidative stress, and fibrosis. Sirtuin family has been shown to be involved in the regulation of fibrosis signaling pathways and in the cellular and molecular mechanisms of liver fibrosis. In this review, we aimed to summarize current knowledge about the signaling pathways that trigger differentiation, profibrotic activation of myofibroblasts and cause liver fibrosis that can be modulated by sirtuins.Publication Metadata only Bariyatrik cerrahi sonrası hibrit egzersiz modelinin vücut kompozisyonu, bazal metabolizma hızı ve kas kuvvetine etkisi(2023-10-07) BAHAR, ASLI NUR; GÜNAL, ÖMER; KASIMAY ÇAKIR, ÖZGÜR; CİNGİ, ASIM; YAVUZ, DİLEK; KÜÇÜK YETGİN, MERAL; Köksalan B., Bahar A. N., Günal Ö., Kasımay Ö., Özbar N., Cingi A., Yavuz D., Küçük Yetgin M.Bariyatrik cerrahi sonrası hibrit egzersiz modelinin vücut kompozisyonu, bazal metabolizma hızı ve kas kuvvetine etkisiBürke Köksalan1, Aslı Nur Bahar2, Ömer Günal3, Özgür Kasımay2, Nurper Özbar4, Asım Cingi3, Dilek Gogas Yavuz5, Meral Küçük Yetgin61 Marmara Üniversitesi, Sağlık Bilimleri Enstitüsü, Hareket ve Antrenman Bilimleri Doktora Programı2 Marmara Üniversitesi, Tıp Fakültesi, Fizyoloji Anabilim Dalı, Spor Fizyolojisi Bilim Dalı3 Marmara Üniversitesi, Tıp Fakültesi, Genel Cerrahi Anabilim Dalı 4 Trakya Üniversitesi, Kırkpınar Spor Bilimleri Fakültesi, Antrenörlük Eğitimi Bölümü, Haraket ve Antrenman Bilimleri Anabilim Dalı5 Marmara Üniversitesi, Tıp Fakültesi, İç Hastalıkları Anabilim Dalı, Endokrinoloji ve Metabolizma Bilim Dalı 6 Marmara Üniversitesi, Spor Bilimleri Fakültesi Antrenörlük Eğitimi Bölümü, Spor Sağlık Bilimleri Anabilim DalıÖzetAmaç: Bu çalışmanın amacı bariatrik cerrahi ameliyatı sonrası uygulanan 4 aylık hibrit egzersiz modelinin vücut kompozisyonu, kas kuvveti ve bazal metabolizma hızı üzerine etkisinin incelenmesidir.Yöntem: Sleeve Gastrektomi (SG) ameliyatı olan 11 gönüllü katılımcı, Hibrit Egzersiz Grubu (HEG/ N=6; VKİ=30,350kg/m2) ve Kontrol Grubu (KG/ n=5; VKİ=33,62 kg/m2) olmak üzere 2 gruba ayrıldı. Programın başında ve sonunda tüm katılımcıların vücut kompozisyonu (Tanita BC-418MA), bazal metabolizma hızı (Cortex Metalyzer 3B), ve kas kuvveti (Lafayette) değerleri alındı. HEG, ameliyattan sonraki 13. haftada başlayarak 4 ay boyunca haftada 3 gün hibrit egzersiz programına tabi tutuldu. Araştırma değişkenlerinin normal dağılım gösterip göstermediğini belirlemek üzere basıklık ve çarpıklık değerleri incelendi. Değişkenlerin normal dağılım gösterdiği belirlendi ve verilerin analizinde parametrik yöntemler kullanıldı. Grup içi ön son test karşılaştırmalarında Paried Samples Test, gruplar arası karşılastırmalarda ise; İndependent Samples T-Tests kullanıldı. Anlamlılık düzeyi p<0.05olarakalındı.Bulgular: Bariatrik cerrahi ameliyatını takiben uygulanan hibrit egzersiz programı sonrasında her iki grubun ön ve son test değerlerinde vücut ağırlığı (HEG=11,790±6,48kg; KG=11,205±5,59kg), VKİ (HEG=12,052±6,482kg/m2; KG=11,214±5,687kg/m2), yağ yüzdesi (HEG=20,381±11,574; KG= 17,467±13,448), yağ kütlesi (HEG=29,085±14,325kg; KG=26,324±15,864kg), yağsız vücut kütlesi (HEG=3,827±2,817kg; KG=3.85±1.942kg) değerlerinde istatistiksel açıdan anlamlı farklılık (p<0,05) bulundu. Ancak gruplar arasında fark elde edilemedi (p>0,05). Bazal metabolizma hızında (HEG=7,329±20,406kcal/d; KG=10,717±10,708kcal/d) grup içi ve gruplar arasında herhangi bir istatistiksel farklılık oluşmadığı belirlendi (p>0,05) HEG grununun kas kuvveti değerine ilişkin ön son test değerlerinde üst sağ ekstremite kuvvet (HEG=33,744±5,442N; KG=2,961±6.276N), üst sol ekstremite kuvvet (HEG=43,573±7,387; KG=2,098±7,165), alt sağ ekstremite kuvvet (HEG=76,802±7,697; KG=12,208±19,921N), alt sol ekstremite kuvvet (HEG=82,486±8,763N; KG=14,122±15,435N) ve gruplar arası yüzdelik gelişimlerinde anlamlı farklılık bulundu (p<0,01). KG grubunda kas kuvveti değerinde grup içi değişimlerde bir farklılık elde edilemedi (p>0,05). Sonuç: Bariatrik cerrahi ameliyatı sonrası uygulanan 4 aylık hibrit antrenman modelinin kas kuvvetini geliştirdiği bulunmuştur. Her iki grupta da vücut kompozisyonu bileşenlerinde görülen anlamlı iyileşme gruplar arasında istatistiksel açıdan bir fark ortaya koymamıştır. Bazal metabolizma hızı değişkeninde gruplar arasında fark ortaya çıkmamıştır. Bariatrik cerrahi sonrası hızlı kilo verme döneminde uygulanan hibrit egzersiz modelinin hastaların kas kuvvetini arttırarak yaşam kalitesini iyileştirmeye katkı sağlayacağı sonucuna varılmıştır. Anahtar kelimeler: Slevee gastrektomi, hibrit egzersiz, bazal metabolizma,kas kuvvetiPublication Metadata only Effect of SIRT2 Inhibition on Developing Fibrosis in D-Galactose-Induced Aging Model(2023-01-05) BAHAR, ASLI NUR; Bahar A. N., Keskin Aktan A., Sonugür F. G., Akarca Dı̇zakar. S. Ö., Akbulut K. G.AIM: Aging is a risk factor for fibrosis and liver injury. SIRT2 inhibition has been shown to have a protective effect on the mechanism of renal interstitial fibrosis. In our study, it was aimed to determine the effect of SIRT2 inhibition by AGK-2 on liver functions and its role in the fibrosis process in the aging model caused by D-galactose (D-GAL).METHODS: A total of 32 3-month-old Sprague Dawley rats were used in the study. Rats were divided into 4 groups as Control, D-GAL, Solvent+D-GAL, D-GAL+AGK2+Solvent. D-galactose (150 mg/ kg/day), AGK-2 (10μM/bw) as a specific SIRT2 inhibitor, 4%DMSO+PBS as a solvent were applied to the experimental groups and physiological saline was applied to the control group for 10 weeks. Biochemical parameters (ALT, AST, platelet count, LDH, HDL, VLDL, total cholesterol, triglyceride) were measured in plasma.AST-ALT Ratio, AST-Platelet Ratio Index (APRI), liver index (liver weight/body weight) were calculated. SIRT2 levels in liver tissues were determined by western blot (WB) and immunohistochemical (IHC) analysis.The expression level of TGF β, β catenin, PDGFBB genes was determined by real-time-polymerase chain reaction. Histopathological scoring was performed to detect tissue damage.For statistical analysis, the data obtained from the study were presented as \"mean±standard deviation\".One-way ANOVA (post-hoc LSD) test was used to determine the intergroup differences, and Pearson correlation test was used to determine the relationshipsbetween the variables(p<0.05). RESULTS: D-Galactose administration increased AST, AST-ALT ratio, APRI, SIRT2 protein expression, TGF β, β catenin mRNA levels in liver tissue. AGK-2 application decreased all theseparameters. SIRT2 expression (WB) is positively correlated with AST,APRI index, TGF β1, β-catenin mRNA expression. SIRT2(IHC) is positively correlated with AST/ALT and APRI index.CONCLUSION: It is thought that SIRT2 inhibition may be effective in improving aging-related fibrotic changes in the liver and preventing aging-related loss of function.Keywords:D-Galactose, Fibrosis, SIRT2 inhibition, TGFβ, β catenin,Liver.Publication Open Access Cerebellum and oxidative stress in natural and accelerated aging model(2023-01-05) BAHAR, ASLI NUR; Kavak H., Bahar A. N., Keskin Aktan A., Akbulut K. G.AIM: Intracerebroventricular administration of galactose causes motor coordination deficiency by decreasing glutathione (GSH) level in the cerebellum. It has been shown that aging increases oxidative stress and Sirtuin 2 (Sirt2) expression in rat cerebellum tissue and Sirt2 inhibition has a protective effect in aging. In our study, we aimed to investigate the effect of AGK-2 administration, a specific Sirt2 inhibitor, on oxidative stress in an accelerated aging model with natural and D-galactose (D-GAL) administration.METHODS: In the study, 7 groups were formed using 48 male rats of Wistar (W) and Sprague-Dawley (SD) species;1) Young-Control (3 months, n=6), 2) Young-AGK-2 (3 months, n=6), 3) Old-Control (22 months, n=6), 4) Old-AGK-2 (22 months, n=6), 5) D-GAL (3 months, n=9), 6) Solvent+D-GAL (3 months, n=8), 7) Solvent+D-GAL+AGK-2 (3 months, n=7). Control groups were given 4% DMSO+PBS, and experimental groups were given AGK-2 (10 μM/bw) subcutaneously (SC). For the accelerated aging model, D-galactose (150 mg/kg/day, SC) was administered for 10 weeks. Malondialdehyde (MDA) and GSH levels in cerebellum tissue were measured by spectrophotometric method.In the statistical analysis, one-way ANOVA (post-hoc LSD) was used to determine the differences between groups. The statistical significance level was set at p<0.05.RESULTS: The D-GAL administration increased the cerebellum MDA level significantly compared to the young control group (p<0.001). In the D-GAL group, AGK-2 administration decreased the MDA levels and increased the GSH levels (p=0.003; p=0.006). D-GAL administration increased MDA levels more and decreased GSH levels significantly compared to aged rats (p=0.006; p<0.001). AGK-2 administration in natural aging was found to be more effective in increasing GSH levels compared to the accelerated aging model (p<0.001).CONCLUSION: Both models compared increased oxidant stress in the cerebellum. AGK-2 application was found to be more effective than D-GAL on oxidant stress in natural aging.Keywords:AGK-2, Accelerated aging, Cerebellum, D-galactose, Natural aging, Oxidative StressPublication Open Access Protective effect of pharmacological SIRT2 inhibition on renal dysfunction, fibrosis, TGF-β1/β-catenin, and klotho signaling in D-galactose-induced aging model(2023-12-01) BAHAR, ASLI NUR; Keskin Aktan A., Bahar A. N., Sonugür F. G., Akarca Dizakar S. Ö., Akbulut K. G.AbstractBackground: Fibrosis induced by transforming growth factor-β1 (TGF-β1) activity and the Wnt/β-catenin pathway is a significant hallmark of progressive kidney disease and kidney aging. We aimed to investigate the effects of pharmacological silent mating type information regulation 2 homolog-2 (SIRT2) inhibition on renal functions, histopathological changes, fibrosis, TGF-β1/β-catenin and klotho signaling, and apoptosis in D-galactose (D-Gal)-induced aging model.Methods: The study was conducted with three months old male rats divided into four groups: control (Saline solution (0.9%, 0.5 mL/day) was administered subcutaneously (sc) for ten weeks) (n = 6), D-Gal (D-galactose saline solution (150 mg/kg/day) was administered sc for ten weeks) (n = 8), D-Gal+DMSO (D-galactose (150 mg/kg/day) and 4% dimethyl sulfoxide (DMSO) in phosphate-buffered saline (PBS) (10 μL/bw/day) were administered sc for ten weeks) (n = 8), and D-Gal+acylglycerol kinase (AGK)-2 (D-galactose (150 mg/kg/day) and AGK-2 in 4% DMSO-PBS (10 μM/bw/day) was administered sc for ten weeks) (n = 8). The kidney index was calculated, renal function markers (sodium (Na+), creatinine (Cr), blood urea nitrogen (BUN)) in plasma and urine samples were analyzed, and fractional excretion of sodium (FeNa%) was calculated. Glomerular diameter, fibrosis, and basement membrane thickness were analyzed with histopathological methods. TGF-β1 and β-catenin mRNA expression were determined with quantitative real-time polymerase chain reaction (qRT-PCR), klotho protein levels were determined with the enzyme linked immunosorbent assay (ELISA) method, and SIRT2 protein expression was determined with western blot. The immunohistochemical method was employed to determine the immunoreactivities of β-catenin, klotho, SIRT2, and fibronectin. Apoptosis was determined with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) method.Results: AGK-2 and D-galactose co-administration increased kidney index and decreased plasma and urine Na+and Cr levels, as well as BUN and FeNa% (p <0.05). AGK-2 improved the histopathological changes induced by D-galactose, reducing fibrosis and basal membrane thickness (p <0.05). Furthermore, AGK-2 administration decreased TGF-β1, β-catenin, SIRT2, and fibronectin in the kidney (p <0.05). AGK-2 and D-galactose co-administration increased klotho protein levels in the kidney; however, the increase was not statistically significant in klotho immunoreactivity (p >0.05). D-galactose induced apoptosis in the kidney (p <0.05); however, AGK-2 did not significantly mitigate apoptosis (p >0.05).Conclusion: Our findings suggested that pharmacological SIRT2 inhibition could ameliorate alterations in functional, histopathological, and fibrosis protein pathway activities in the kidney that are associated with aging.Key wordsD-galactose/fibrosis/kidney/SIRT2 inhibition/TGF-β1