Browsing by Author "Arici, Mualla Aylin"

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Citation - WoS: 2
Citation - Scopus: 2
Preventative Effect of Montelukast in Mild To Moderate Contrast-Induced Acute Kidney Injury in Rats Via Nadph Oxidase 4, P22phox and Nuclear Factor Kappa-B Expressions
(Springer, 2025) Simsek, Oguzhan; Baris, Elif; Ural, Cemre; Incir, Canet; Aydemir, Selma; Gumustekin, Mukaddes; Arici, Mualla Aylin
Reactive oxygen species (ROS) generation, inflammation and apoptosis are observed in contrast-induced acute kidney injury (CI-AKI). NOX4, isoform of NADPH oxidase main regulatory enzyme for ROS generation, is mostly expressed in the kidney and co-localized with p22phox. It is investigated the effect of antioxidant, anti-inflammatory and anti-apoptotic montelukast pre-treatment on expression of NOX4, p22phox and NF-kappa B in preventing CI-AKI in rats in this study. Wistar male rats randomized into four groups: 1. Control (C), 2. CI-AKI (iohexol; 3 g iodine/kg), 3. Montelukast (10 mg/kg) (M), 4. M + CI-AKI. Rats sacrificed on the 7th day. Urine and serum creatinine and serum Kidney injury molecule-1 (KIM-1) levels measured. NF-kappa B, NOX-4, p22phox mRNA and protein expressions, TNF-alpha, KIM-1 mRNA expressions, ROS and caspase-3 evaluated from kidney tissue. Histological injury scored. ANOVA and Kruskal-Wallis tests were used for analysis parametric and nonparametric data, respectively. p < 0.05 considered statistically significant. Tubular injury score, KIM-1 and caspase-3 levels increased in CI-AKI group compared to C group (p < 0.05). TNF-alpha, NF-kappa B, NOX-4, p22phox, KIM-1 mRNA expressions and ROS levels increased in CI-AKI group compared to C group (p < 0.001 and p < 0.05). NF-kappa B, NOX-4, p22phox protein expressions increased in CI-AKI group compared to C group (p < 0.05) and decreased in the M + CI-AKI group compared to CI-AKI group (p < 0.01, p < 0.05, p < 0.05). TNF-alpha, NF-kappa B, NOX-4, p22phox, KIM-1 mRNA expressions and ROS levels decreased with montelukast pre-treatment (p < 0.001). One of the mechanism of increased ROS level in the CI-AKI model is related the increase the expression of NOX4 and p22phox and montelukast pre-treatment has a protective effect by decreasing NOX4 and p22phox mRNA and protein expressions.
Citation - WoS: 1
The Role of Nicotinic Anti-Inflammatory Pathway in Prostaglandin Mediated Inflammatory Response in Sepsis: a Short Review
(Marmara Univ, Inst Health Sciences, 2019) Baris, Elif; Arici, Mualla Aylin; Hamurtekin, Emre
Sepsis is a severe and multifaceted condition of body in response to an infection, which affects multiple organs systems that makes it difficult to treat and enhances the mortality rates. Release of inflammatory cytokines can initiate an inflammatory response during sepsis. However, the response can be modified by the control mechanism inside the body that are essential for the keeping the balance and survival. The cholinergic anti-inflammatory pathway is defined as a comprehensive neurohumoral pathway that diminishes pro-inflammatory cytokine release through the vagus nerve and cholinergic receptors, predominantly alpha 7 nicotinic acetylcholine receptors (alpha 7nAChR) that expressed on inflammatory mononuclear cells. Thus, cholinergic agonists might be a part of prospective treatment approach in inflammatory diseases such as sepsis. This review covers the role of cholinergic system in prostaglandin mediated inflammatory response.
Citation - WoS: 2
Citation - Scopus: 3
Serum Choline, Leptin and Interleukin-6 Levels in Fibromyalgia Syndrome-Induced Pain: a Case-Control Study
(Bmc, 2025) Baris, Elif; Topaloglu, Izel; Akalin, Elif; Hamurtekin, Emre; Kabaran, Seray; Gelal, Ayse; Arici, Mualla Aylin
Background Fibromyalgia Syndrome (FMS) predominantly affects middle-aged women, characterized by musculoskeletal pain, fatigue, and cognitive issues. Choline, an endogenous molecule, may influence FMS due to its analgesic and anti-inflammatory properties. This study compared choline, leptin, and interleukin-6 (IL-6) levels in FMS patients and controls and examining their association with pain severity. Methods Volunteers with FMS were clinically diagnosed at a Physical Medicine and Rehabilitation Department. The control group included pain-free volunteers. Pain severity was gauged using a numeric scale, dietary choline intake through a questionnaire. Serum choline, leptin and (interleukin)IL-6 levels were measured from fasting blood samples of volunteers with enzyme-linked immunosorbent assays (ELISA). Results All FMS patients (n = 38) and healthy volunteers (n = 38) were female. Pain score in patients with FMS was 7.6 +/- 0.2. Dietary choline intake was lower in patients with FMS than the controls (p = 0.036). Serum choline and leptin levels were lower in the FMS group compared to control (p = 0.03). Serum IL-6 levels were higher in the FMS group than in the control (p < 0.001). There was weak positive correlation between IL-6 levels and pain scores and there were no correlation between leptin levels and pain scores in FMS. Conclusions This research highlights FMS's complex nature, involving neurochemical, immunological, and nutritional factors. It suggests the significance of choline's anti-inflammatory effect, leptin's metabolic function, and IL-6's role in FMS pathology. The results suggest that reduced dietary choline might influence serum choline, leptin, and IL-6 levels, potentially impacting FMS-related pain. This points to the potential of supplementary choline intake in FMS management. Trial registration Not applicable (Non-interventional study).
Citation - WoS: 11
Citation - Scopus: 11
Varenicline Prevents Lps-Induced Inflammatory Response Via Nicotinic Acetylcholine Receptors in Raw 264.7 Macrophages
(Frontiers Media Sa, 2021) Baris, Elif; Efe, Hande; Gumustekin, Mukaddes; Arici, Mualla Aylin; Tosun, Metiner
The cholinergic anti-inflammatory pathway plays an important role in controlling inflammation. This study investigated the effects of varenicline, an alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR) agonist, on inflammatory cytokine levels, cell proliferation, and migration rates in a lipopolysaccharide (LPS)-induced inflammation model in RAW 264.7 murine macrophage cell lines. The cells were treated with increasing concentrations of varenicline, followed by LPS incubation for 24 h. Prior to receptor-mediated events, anti-inflammatory effects of varenicline on different cytokines and chemokines were investigated using a cytokine array. Nicotinic AChR-mediated effects of varenicline were investigated by using a non-selective nAChR antagonist mecamylamine hydrochloride and a selective alpha 7nAChR antagonist methyllycaconitine citrate. TNF alpha, IL-1 beta, and IL-6 levels were determined by the ELISA test in cell media 24 h after LPS administration and compared with those of dexamethasone. The rates of cellular proliferation and migration were monitored for 24 h after drug treatment using a real-time cell analysis system. Varenicline decreased LPS-induced cytokines and chemokines including TNF alpha, IL-6, and IL-1 beta via alpha 7nAChRs to a similar level that observed with dexamethasone. Varenicline treatment decreased LPS-induced cell proliferation, without any nAChR involvement. On the other hand, the LPS-induced cell migration rate decreased with varenicline via alpha 7nAChR. Our data suggest that varenicline inhibits LPS-induced inflammatory response by activating alpha 7nAChRs within the cholinergic anti-inflammatory pathway, reducing the cytokine levels and cell migration.