Browsing by Author "Gokdemir, Gul Sahika"

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Analysis of Microorganisms Isolated from Tracheal Aspirate Cultures and Their Antibiotic Susceptibility Profiles: A Retrospective Study from 2018 to 2022
(Frontiers Media SA, 2026) Sanmak, Erkan; Cil, Baris; Ayaydin, Zeynep; Canbaz, Hayri; Davarci, Ismail; Gokdemir, Gul Sahika; Guler, Gokhan
Background: To determine the distribution of microorganisms isolated from tracheal aspirate (TA) cultures and their antimicrobial susceptibility patterns, and to assess resistance differences between intensive care unit (ICU) - and ward-derived isolates as well as temporal trends across years. Methods: Tracheal aspirate specimens obtained at a tertiary-care center between 2018 and 2022 were retrospectively reviewed. Only growth meeting laboratory acceptance criteria for causative pathogens was analyzed (semi-quantitative culture thresholds with cytologic quality control). Bacterial identification was performed using automated systems, and antimicrobial susceptibility testing was interpreted according to EUCAST standards. In addition to descriptive analyses, annual resistance trends and a joinpoint regression analysis (annual percent change) were conducted. Results: Of all causative isolates, 83.8% were Gram-negative. The most frequent pathogens were Klebsiella spp., Acinetobacter spp., and Pseudomonas spp. For Klebsiella spp., resistance to cephalosporins and fluoroquinolones was generally >90%, meropenem >80%, whereas imipenem showed comparatively higher susceptibility. In Acinetobacter spp., resistance was very high to most agents, with amikacin showing the lowest resistance. In Pseudomonas spp., resistance rates ranged from 40% to 55%, and amikacin emerged as the most active agent. Resistance was systematically higher in ICU-derived isolates than in ward isolates. Joinpoint analysis identified a single breakpoint around 2020; resistance trajectories during 2018-2020 were heterogeneous, with increases observed for some organism-antimicrobial combinations, followed by divergent patterns thereafter. Conclusion: The predominance of Gram-negative pathogens and the high resistance burden in our center support locally tailored Gram-negative coverage for empiric therapy alongside early de-escalation. Temporal patterns underscore the need to update empiric policies using annual local surveillance data and to reinforce infection control and antimicrobial stewardship, particularly in ICUs.
Citation - WoS: 1
Citation - Scopus: 1
Antidepressant-Like Effects of Ashwagandha (Withania Somnifera) on Chronic Unpredictable Mild Stress-Induced Depression in Adolescent Rats
(Springer, 2025) Gokdemir, Gul Sahika; Seker, Ugur; Baksi, Nazan; Baylan, Mukadder; Demirtas, Berjan; Gokdemir, Mehmet Tahir
RationaleAdolescent depression is often linked to biological changes associated with stress. However, new approaches and treatment strategies for early intervention and prevention of depression in children and adolescents are still limited. Ashwagandha is an Ayurvedic herb widely used in the management of anxiety and stress. However, there is no information in the current literature on its potential effect on adolescent depression.ObjectivesThis study aimed to investigate the effects of depression on proapoptotic proteins and neuroinflammation and the antidepressant effect of Ashwagandha on depression-like symptoms in adolescent rats exposed to the Chronic Unpredictable Mild Stress (CUMS) model.MethodsIn the study, CUMS model was used to induce depression in adolescent rats. Rats were treated with Ashwagandha or Sertraline. To evaluate the antidepressant effects, behavioral tests as well as biochemical and histological analyses were performed. Forced Swim Test (FST), Sucrose Test and Elevated Plus Maze Test were performed as behavioral tests. Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were measured by the ELISA method in the fronto-parietal cortex. Proapoptotic proteins (Bax and Caspase-3) and inflammatory markers (TNF-alpha and IL-1 beta), as well as glial fibrillary acidic protein (GFAP), were evaluated immunohistochemically in the fronto-parietal cortex.ResultsProapoptotic proteins (Bax and Caspase-3) and inflammatory markers (TNF-alpha and IL-1 beta) were increased in the CUMS group. BDNF and GFAP levels were decreased. Ashwagandha treatment was more effective than Sertraline in reducing the levels of these proteins and markers. Additionally, Ashwagandha prevented weight loss.ConclusionsAshwagandha showed antidepressant-like effects in adolescent rats, reducing apoptosis, inflammation, and neuroinflammation, suggesting potential for treating adolescent depression.
Citation - WoS: 2
Citation - Scopus: 2
Assessment of Iron Metabolism and Inflammation in Children With Cerebral Palsy
(Mdpi, 2025) Orhan, Ozhan; Gokdemir, Gul Sahika
Background/Objectives: Cerebral palsy (CP) is a motor disorder resulting from brain damage that is common in childhood. Iron is vital for the body's basic functions. Iron metabolism disorders and inflammation contribute to the neurological complications seen in CP. The purpose of this research was to ascertain the association and correlation between markers of inflammation and iron metabolism in children with CP. Methods: A total of 181 children diagnosed with CP and 111 typically developing children were retrospectively included in the study. Demographic data, blood parameters, C-reactive protein, iron, total iron binding capacity, and inflammation markers were evaluated. Results: C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR) and systemic immuno-inflammatory index (SII) levels of CP children were found to be statistically significantly higher than those of control group children (p < 0.05). Iron (Fe) and ferritin levels were lower in the CP group, while total iron binding capacity (TIBC) was higher. Spearman correlation analysis showed significant correlations between iron, ferritin and TIBC and SII. Conclusions: Iron deficiency and chronic inflammation are associated with the pathophysiology of CP in patients with CP, and therefore it is important to monitor markers of iron metabolism and inflammation in these patients.
Cadmium-Induced Systemic Inflammation and Retinal Degeneration: Histopathological and Cytokine Analysis in a Rat Model
(Taylor & Francis Ltd, 2026) Gokdemir, Gul Sahika; Demirtas, Selim; Seker, Ugur
Clinical RelevanceCadmium causes systemic inflammation and retinal damage, posing a serious threat to visual and public health.BackgroundCadmium is a harmful heavy metal that builds up in body tissues and cause systemic inflammation and organ damage. This research sought to explore the impact of subacute cadmium exposure on retinal morphology and inflammatory cytokine levels.MethodA total of fourteen male Wistar albino rats were randomized into control and cadmium-exposed groups within the scope of the experiment. 3 mg/kg cadmium (CdCl2) was administered intraperitoneally to the subjects in the cadmium group for 15 days. At the end of study, serum IL-6 and TNF-alpha levels were determined by ELISA method. In addition, retinal tissues were examined histopathologically after Hematoxylin and Eosin staining. Retinal apoptotic changes were assessed by semi-quantitative immunohistochemical analysis of Bax and Bcl-2 expression in the inner and outer nuclear layers.ResultsAccording to the findings, cadmium exposure caused a statistically significant increase in serum IL-6 and TNF-alpha levels. Histopathological examination revealed a marked decrease in the thickness of the inner plexiform layer (IPL), inner nuclear layer (INL), and outer nuclear layer (ONL), as well as focal vacuolization and cellular disorganization. Cadmium exposure significantly increased Bax immunoreactivity and the Bax/Bcl-2 ratio in both the INL and ONL, while significantly decreasing Bcl-2 expression.ConclusionIn conclusion, cadmium exposure increased the systemic inflammatory response, leading to significant histopathological damage in the retinal layers and a dominant proapoptotic Bax/Bcl-2 balance, thereby triggering cellular apoptosis.
Covid-19 Hastalarında HDL-K Değerinin Rutin İnflamasyon Parametreleri olan h-CRP,Lenfosit ve Nötrofil Oranlarının Klinik Önemi
(2023) Gokdemir, Gul Sahika; Nas, Cemal
Amaç: Bu çalışma, nötrofil/HDL-C oranı (NHR) ve lenfosit/HDL-K oranı (LHR) gibi belirteçlerin yanı sıra yüksek yoğunluklu lipoprotein kolesterol (HDL-K) seviyelerinin COVID-19 hastalarının mortalitesi üzerindeki prognostik önemini değerlendirmeyi amaçlamıştır. Ayrıca, COVID-19 pandemisinin sona ermesine rağmen, bu biyobelirteçlerin gelecekteki sağlık krizlerinin yönetiminde potansiyel klinik uygulamalarını da incelemiştir. Gereç ve Yöntemler: COVID-19 tanısı konan hastalar Mart 2020 ile Ağustos 2022 tarihleri arasında retrospektif olarak analiz edilmiştir. Toplam 367 hasta iki gruba ayrılmıştır: hayatta kalanlar (grup 2) ve hayatta kalmayanlar (grup 1). Hasta demografisi, kan örneklerinden elde edilen biyokimyasal ve hematolojik parametreler, yüksek hassasiyetli C-reaktif protein (hs-CRP), nötrofil-lenfosit oranı (NLR), monosit/HDL-K oranı (MHR), NHR, LHR, trombosit/HDL-K oranı (PHR) hesaplanmıştır. Hasta verileri SPSS 26 kullanılarak analiz edildi ve P<0.05 olan istatistiksel farklılıklar anlamlı kabul edildi. Bulgular: Çalışmada analiz edilen hastalar arasında yaşayan grup bireylerin %89,9'unu oluştururken, vefat eden grup %10,1'ini temsil etmektedir. Nötrofil düzeyleri ölen grupta anlamlı olarak daha yüksekti ve NLR ve NHR değerleri istatistiksel olarak anlamlıydı (sırasıyla P<0,001 ve P=0,001). HDL-K düzeylerinde herhangi bir farklılık yoktu. LHR, MHR ve PHR değerlerinde gruplar arasında anlamlı bir farklılık gözlenmedi. Hs-CRP düzeyleri ölenlerde anlamlı olarak daha yüksekti (P<0.001). Korelasyon analizi HDL-K ile LHR ve NHR arasında negatif korelasyon olduğunu gösterirken, diğer belirteçler için anlamlı korelasyonlar bulunmuştur. ROC analizi LHR ve NHR'nin ölen hastaları ayırt etmede anlamlı olduğunu göstermiştir. Sonuçlar: Biyokimyasal ve hematolojik parametreler, özellikle NLR ve NHR gibi belirteçler, COVID-19 hastalarında ölüm riskini değerlendirmek için potansiyel olarak kullanılabilir. Bu belirteçler hastaların prognozunu tahmin etmede değerli olabilir ve gelecekteki benzer sağlık krizlerinde kullanılabilir.
Dose-Dependent Hepatotoxicity of Diethyl Phthalate in Female Wistar Rats
(MDPI, 2026) Tan, Fazile Canturk; Gokdemir, Gul Sahika; Kalkan, Kubra Tugce; Varol, Salih; Yavas, Mehmet Cihan; Cantürk Tan, Fazile
Phthalates are a class of compounds commonly used as plasticizers in various industrial and consumer products. In line with the increasing environmental and biological exposure concerns regarding these compounds, this study investigated the dose-dependent effects of diethyl phthalate (DEP) on the liver in a subacute rat model. Diethyl phthalate (DEP) was given orally by gavage to female Wistar albino rats at doses of 100, 300, and 600 mg/kg body weight per day for 21 days in order to assess liver tissue and associated function test levels. Liver function was evaluated by analyzing serum biochemical data. Liver tissues were evaluated using histopathological staining (H&E and Masson's trichrome staining), immunohistochemical analysis of IL-1 beta and TGF-beta, tissue ELISA for IL-6 and TNF-alpha, and comet assay to determine DNA damage. DEP exposure was found to cause significant, dose-dependent histopathological changes in liver tissue, including hepatocyte necrosis, cytoplasmic vacuolization, sinusoidal dilation, and vascular congestion. AST levels were significantly increased compared to the control group, while no significant changes were observed in other serum biochemical parameters. Compared to the control group, the expression of pro-inflammatory cytokines (IL-6 and TNF-alpha), IL-1 beta, and TGF-beta was found to be elevated in the DEP-treated groups, and their levels increased with increasing exposure dose. DEP exposure also caused significant DNA damage in liver tissue. These findings indicate that despite an increase in AST levels observed in subacute DEP exposure, there were limited changes in serum biochemical parameters; serum liver enzymes alone may not fully reflect the extent of hepatic damage, and DEP can cause significant inflammatory, histopathological, and genotoxic effects in liver tissue.
Citation - WoS: 1
The Effect of Acute Carbon Monoxide Intoxication on Cardiac Necrosis in Rats: in Relation To Adiponectin Levels
(Univ Zulia, Facultad Ciencias veterinarias, 2025) Gokdemir, Gul Sahika; Cakmak, Sumeyye; Demirtas, Berjan; Gokdemir, Mehmet Tahir; Sogut, Ozgur; Canpolat-Erkan, Revsa Evin; Yokus, Beran
In order to investigate the effects of acute CO poisoning and subsequent oxygen therapy on cardiac necrosis in rats, with a specific focus on adiponectin levels, twenty-one male Wistar albino rats were divided into three groups (Control, CO, CO+O-2). The Control group was placed in a container and exposed to room air for 30 min. Acute CO poisoning was induced in the CO group and CO+O-2 group by exposing the rats to CO gas for 30 min. Following CO exposure, the CO+O-2 group received oxygen therapy for 30 min, while the CO group did not receive any additional intervention. The animals were euthanized by cardiac puncture under anesthesia, following the approved ethical procedures. Carboxyhemoglobin (COHb), serum levels of creatine kinase (CK), creatine kinase myocardial band (CK-MB), C-reactive protein (CRP) and lactate dehydrogenase (LDH), as well as cardiac and serum adiponectin levels were measured. CO poisoning caused necrosis in cardiac tissue however, oxygen therapy alleviated the negative effect of CO on cardiac injury. COHb and LDH levels in CO group were increased, whereas both cardiac and serum adiponectin levels were decreased (all, P<0.05). There were no changes in CK, CK-MB, CRP levels among groups (all, P>0.05). Oxygen therapy decreased COHb, but increased both cardiac and serum adiponectin levels (all, P<0.05). Adiponectin and LDH may serve as potential biomarkers for early diagnosis of cardiac necrosis caused by acute CO poisoning. The assessment or quantification of adiponectin can also be useful for the early prognosis of cardiac necrosis after oxygen therapy.
The Effect of Gliclazide Use on BDNF and NGF Levels in Rats with Diabetes Mellitus
(2023) Gokdemir, Gul Sahika; Atmaca, Mukadder
Objective: In this study, the effects of gliclazides, a second generation sulfonylurea group, on BDNF and NGF plasma levels, which are considered neurodegeneration biomarkers, will be examined. When designing our study, we assumed that gliazides might have positive neu- ronal effects. Thus, the possible positive effects of gliclazide will be emphasized in our study. Methods: In the experiment, 21 adult male Wistar-Albino rats were used. Serum BDNF and NGF levels were determined by analyzing with enzyme-linked immunosorbent assay kit in accordance with the recommendations. Results: BDNF levels were significantly lower in gliclazide-treated diabetic rats and non- medicated diabetic rats compared to the healthy control group (p=0.017, p<0.001, re- spectively). Although the BDNF level of rats with diabetes given gliclazide was increased compared to rats with and without diabetes, this difference was not significant (p=0.107). Similarly, NGF levels were significantly lower in rats given gliclazide (p=0.009) and diabetic rats not given gliclazide (p=0.001) compared to the healthy control group. When the dia- betic groups were compared among themselves, although the NGF level was increased in the gliclazide group, this difference was not statistically significant (p=0.638). The differences between the groups were significant in cyclic AMP regulatory element binding (p<0.001), c-FOS (p<0.001), amyloid precursor protein (p<0.001), B-SECRETASE1 (p=0.004), and dou- blecortin (p<0.001) levels. Conclusion: As a result, serum BDNF and NGF levels were significantly higher in non-dia- betic healthy control group rats than in diabetic rats. While low serum levels of BDNF and NGF neurotrophins, which increase in neurodegeneration, were observed in diabetic rats, this level was observed to be higher in diabetic rats given gliclazide.
Citation - WoS: 6
Citation - Scopus: 5
Effects of Acute Carbon Monoxide Poisoning on Liver Damage and Comparisons of Related Oxygen Therapies in a Rat Model
(Taylor & Francis Ltd, 2024) Demirtas, Berjan; Taskin, Seyhan; Gokdemir, Gul Sahika; Seker, Ugur
Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% NBO with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction. [GRAPHICS] .
Effects of Gilaburu Fruit Extract on Cardiomyopathy in Diabetic Rats
(2025) Seker, Ugur; Gokdemir, Gul Sahika; Demirtaş, Selim
Objective: The effects of diabetes on cardiomyopathy have been well documented in the literature. However, the effects of gilaburu fruit, which possesses antioxidant and anti-inflammatory properties, on diabetic cardiomyopathy (DCM) have not been adequately investigated. This study aimed to investigate the effects of gilaburu extract on DCM in diabetic rats. Method: Twenty-one male Wistar rats were divided into three groups. Diabetes was induced in the diabetic group with a single intraperitoneal (i.p.) injection of streptozotocin (STZ) at a dose of 50 mg/kg. The treatment group received gilaburu extract (200 mg/kg, i.p.) dissolved in phosphate buffer saline (PBS) for 37 days, starting one week before diabetes induction. Serum CK-MB and CRP levels, cardiac tissue MDA, SOD, and IL-1ß levels, as well as histopathological changes such as hypertrophy, vacuolization, and fiber disarray, were evaluated. Results: Serum CK-MB and CRP levels were significantly higher in the diabetic group compared to the control group. The diabetic group also exhibited marked myocardial hypertrophy, vacuolization, and fiber disarray, along with increased MDA and IL-1ß levels and decreased SODactivity. In the treatment group, CK-MB and CRP levels were significantly reduced, histopathological alterations were markedly attenuated, and MDA, IL-1ß, and SOD levels improved to values close to those of the control group. Conclusion: Gilaburu extract exhibits both biochemical and morphological protective effects against diabetic cardiomyopathy. These findings suggest that gilaburu may be a promising therapeutic agent for the management of diabetic cardiomyopathy.
High-Flow Nasal Cannula Oxygen Versus Conventional Oxygen Therapy in a Rat Model of Severe Carbon Monoxide Toxicity
(MRE Press, 2025) Cakmak, Sumeyye; Gokdemir, Gul Sahika; Gokdemir, Mehmet Tahir; Sogut, Ozgur; Erkan, Revsa Evin Canpolat
Background: This study compared the efficacy of high-flow nasal cannula (HFNC) oxygen therapy with conventional oxygen therapy (COT) using a simple face mask for clearing carbon monoxide (CO) from the bloodstream in a rat model of severe CO poisoning. Methods: Twenty-eight male Wistar rats were assigned to four groups: severe CO intoxication treated with HFNC, a sham group (no intoxication or treatment), severe CO intoxication treated with COT, and a control group with severe CO intoxication receiving no treatment. Their arterial blood gas and metabolic parameters were analyzed and compared to determine treatment effectiveness. Results: Significant differences were observed among the groups in terms of carboxyhemoglobin (COHb), pH, bicarbonate (HCO3), hemoglobin, sodium (Na), potassium (K), calcium (Ca), glucose and lactate levels. Both treatment groups had lower COHb and lactate levels compared to the untreated control group, with COHb clearance being significantly higher in the HFNC group than in the COT group (20.33% +/- 3.58% vs. 41.17% +/- 6.49%; p < 0.001). Additionally, pH levels were higher in the HFNC group than in the COT group (7.32 +/- 0.07 vs. 7.27 +/- 0.05; p = 0.486). Conclusions: HFNC oxygen therapy was found to be more effective than COT in promoting CO elimination and improving arterial blood gas parameters, indicating its potential as a superior treatment strategy for severe CO poisoning.
Importance of Curcumin Effect and Asprosin Level on Glucose Metabolism in Diabetic Rats
(2023) Gökdemir, Mehmet Tahir; Taşdemir, Ezel; Yokus, Beran; Atmaca, Mukadder; Gokdemir, Gul Sahika
Asprosin is a new hormone secreted mainly from white adipose tissue. It may be associated with the pathogenesis of obesity, diabetes and some metabolic diseases. The changes in plasma asprosin levels of experimental diabetic rats and the relation of these changes with liver glucose metabolism and some diabetes parameters were investigated, and the effects of metformin, gliclazide or curcumin treatment on plasma asprosin levels were tried. The study was designed as an animal model in diabetic rats The albino rats were divided into five groups. To induce diabetes, a single dose of STZ was injected intraperitoneally. Diabetics rats were treated intragastrically with metformin (D+Metformin group), gliclazide (D+Giliclazide group) or 20 curcumin (D+Curcumin group) for eight weeks. Fasting blood glucose, insulin levels and other parameters were measured. Plasma asporsin levels of untreated diabetic rats increased significantly (P<.001). Although the plasma asprosin levels of diabetic rats treated with the rugs were significantly lower (P<.001). Fasting blood glucose levels of diabetic rats treated with the drugs were found to be remarkably lower than the diabetic control values (P<.001, respectively). There was no significant difference in the insulin levels and HOMA- IR between these three groups. Curcumin treatment provides significant improvements in plasma asprosin level and diabetes parameters. The increase in plasma asprosin level in diabetic rats may be one of the main reasons that facilitate the development of the disease or is responsible for its pathogenesis. Our findings support the idea that curcumin may be an important treatment option for diabetes.
The Importance of Serum Vitamin B12, Folic Acid and Ferritin Levels in Acute Ischemic Stroke Patients
(Wiley, 2023) Gokdemir, Gul Sahika
[No Abstract Available]
Citation - WoS: 4
Citation - Scopus: 4
The M1/M2 Macrophage Polarization and Hepatoprotective Activity of Quercetin in Cyclophosphamide-Induced Experimental Liver Toxicity
(Wiley, 2025) Seker, Ugur; Uyar, Emre; Gokdemir, Gul Sahika; Kavak, Deniz Evrim; Irtegun-Kandemir, Sevgi
Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs. Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)-induced liver toxicity. Methods: Twenty-four mice were divided into four groups (Control, QUE, CTX, CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg CTX. The animals in the QUE and CTX + QUE groups received 50 mg/kg QUE. All animals were sacrificed, and serum and liver samples were used for laboratory analyses. Results: Examinations indicated that CTX exposure led to disruption of liver functions and morphological degenerations. Tissue pro-apoptotic Bax and caspase 3, pro-inflammatory TNF-alpha and IL-1 beta, transcription factor NF-kappa B, and M1 macrophage polarization marker CD86 were upregulated significant (p < 0.05) in this group. In addition, CTX exposure led to significantly (p < 0.05) upregulation of the Bax/Bcl-2 mRNA ratio and DNA fragmentations. The PCNA-positive hepatic cell ratio and anti-apoptotic Bcl-2 expression are remarkably suppressed (p < 0.05). Immunohistochemical analyses are also indicated that M2 macrophage polarization marker CD163 is slightly but remarkably (p < 0.05) downregulated in the CTX group compared to the Control and QUE groups. The morphological and biochemical disruptions were alleviated in QUE-treated animals in the CTX + QUE group. Liver function test results, apoptosis, inflammatory, transcription factor NF-kappa B, regeneration/proliferation, and apoptotic index results in this group were similar (p > 0.05) to the control and QUE groups. The M1 cell surface marker expression of CD86 is significantly (p < 0.05) downregulated, and M2 macrophage polarization marker expression of CD163 is upregulated significantly (p < 0.05) compared to the CTX group. Conclusions: This study indicates that QUE has the potential to downregulate CTX-induced hepatic injury and regulate M1/M2 macrophage polarization to the M2 side, which indirectly demonstrates activation of anti-inflammatory signalling and tissue repair.
Nephroprotective Effects of Visnagin through Modulation of Macrophage Polarization, Oxidative Stress, Inflammation and Apoptosis in Renal I/R Injury
(de Gruyter Poland SP z o o, 2026) Pekince-Ozoner, Merve; Seker, Ugur; Kaya, Seval; Yuksel, Meral; Demir, Mehmet; Sagir, Suleyman; Gokdemir, Gul Sahika
Objectives: The study aimed to investigate the nephroprotective effects of visnagin on renal ischemia-reperfusion (I/R) injury and the role of M1/M2 macrophage polarization in this process. Methods: Forty-two adult rats were divided into six groups: Control, Visnagin30 mg/kg, Visnagin60 mg/kg, I/R, I/R + Visnagin30 mg/kg, I/R + Visnagin60 mg/kg (n=7). Bilateral renal ischemia was induced by clamping for 25 min, followed by 2 h of reperfusion. Visnagin or vehicle was administered to the animals intraperitoneally 2 h before reperfusion. At the end of the study, kidney samples were collected for analysis of oxidative stress, inflammatory cytokines, apoptotic protein expression, and M1/M2 macrophage polarization. Results: I/R injury increased malondialdehyde (MDA), chemiluminescence (CL), IL-1 beta, and IL-6 levels while decreasing glutathione (GSH) in renal tissue, indicating enhanced oxidative stress (p<0.001) and inflammation (p<0.05). Histopathological examination showed glomerular atrophy, tubular degeneration, and intertubular hemorrhage. Visnagin treatment at 60 mg/kg significantly reduced MDA, CL, and IL-1 beta levels, and increased GSH (p<0.05). Immunohistochemically, visnagin decreased Bax (p<0.001), caspase-3 (p<0.01), and TNF-alpha (p<0.01) expressions elevated by I/R injury. Furthermore, visnagin reversed I/R induced M1/M2 macrophage polarization (CD86 up arrow, CD163 down arrow), decreasing CD86 (p<0.05) and increasing CD163 immunodensity (p<0.05). Conclusions: Visnagin treatment (60 mg/kg) exerts promising nephroprotective effects in renal I/R injury by reducing oxidative stress, inflammation, apoptosis, and modulating M1/M2 macrophage polarization.