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Öğe Capsaicin Reduces Kidney Injury in a Sepsis Model Induced by Cecal Ligation and Puncture(Wiley, 2025) Bircan, Burak; Firat, Semanur; Cakir, Murat; Sekerci, Guldeniz; Oz, Samet; Aydin, Ali[No abstract available]Öğe The Effect of Capsaicin on Oxidative Stress Parameters in Kidney in Sepsis Model Induced by Cecal Ligation and Puncture(Wiley, 2023) Firat, Semanur; Bircan, Burak; Cakir, Murat; Sekerci, Guldeniz; Oz, Samet[Abstract Not Available]Öğe The Effect of TRPA1 Channel Agonist ASP7663 and Antagonist HC-030031 on Oxidative Stress Parameters in Renal Ischemia Reperfusion in Rats(Wiley, 2023) Firat, Semanur; Sekerci, Guldeniz; Cakir, Murat; Bircan, Burak; Oz, Samet[Abstract Not Available]Öğe Inhibition of Transient Receptor Potential Ankyrin 1 Channels Reduces Renal Ischemia Reperfusion Injury(Wiley, 2025) Firat, Semanur; Cakir, Murat; Bircan, Burak; Aydin, Ali; Sekerci, Guldeniz; Oz, Samet[No abstract available]Öğe JAK inhibitor Baricitinib Attenuates Kidney Injury in Sepsis Model Induced by Cecal Ligation and Puncture(Wiley, 2025) Tarakci, Betul; Firat, Semanur; Cakir, Murat; Bircan, Burak; Sekerci, Guldeniz; Aydin, Ali[No abstract available]Öğe JAK1/JAK2 inhibitor baricitinib ameliorates sepsis-induced acute kidney injury in rats(Elsevier, 2025) Cakir, Murat; Tarakci, Beti; Aydin, Ali; Bircan, Burak; Firat, Semanur; Sekerci, GildenizBackground: Baricitinib (Bar), used in the management of rheumatoid arthritis, is a selective inhibitor of JAK1/ JAK2. Studies have shown that it inhibits the intracellular signaling of many proinflammatory cytokines by suppressing STAT3 activation. Increased expression and activity of JAK1/JAK2 and STAT3 are associated with kidney damage. Here, we examined the effects of the JAK1/JAK2 inhibitor baricitinib (Bar) on kidney damage in a sepsis model created with cecal ligation and puncture (CLP) in rats. Methods: Rats were divided into four groups: control, CLP, CLP + Bar 3 mg kg- 1, and CLP + Bar 10 mg kg- 1. The cecum of animals to which CLP was applied was first ligated distally, then punctured with a needle to allow the fecal content to spread into the abdominal cavity. Two different doses of Bar (3 mg kg- 1, 10 mg kg- 1) were applied to the treatment groups. Biochemical examinations were performed on the sera of animals sacrificed 24 h after CLP, while histopathological and immunohistochemical examinations were performed on kidney tissue. ResultsÖğe Protective Effect of Transient Receptor Potential Ankyrin 1 Inhibition on Renal Ischemia Reperfusion Injury in Rats(Wiley, 2025) Cakir, Murat; Aydin, Ali; Firat, Semanur; Sekerci, Guldeniz; Bircan, Burak; Oz, SametThe transient receptor potential ankyrin 1 (TRPA1) channels, characterized as nonselective cation channels with permeability to calcium ions (Ca2 +), are part of the extensive family of transient receptor potential (TRP) channels. Research has demonstrated that TRPA1 channels function as sensors for oxidative stress in the renal tubules. Additionally, TRPA1 expression has increased in renal tissue following ischemia-reperfusion (IR). There is also a significant correlation between IR-induced renal injury and TRPA1 expression. This study investigated the effects of selective TRPA1 agonist ASP7663 and selective TRPA1 antagonist HC-030031 on renal IR injury. A total of 40 rats were divided into four groups: control, IR, IR+ASP7663, and IR + HC-030031. The rat kidneys were exposed to 45 min of ischemia, followed by 24 h of reperfusion. TRPA1 agonist ASP7663 and selective TRPA1 antagonist HC-030031 were administered intraperitoneally to the treatment groups with renal IR. HC-030031 administration reduced the elevated kidney injury molecule-1 (KIM-1), blood urea nitrogen (BUN), and creatinine (Cre) caused by renal IR. HC-030031 administration reduced the increased histopathological damage in renal tissue due to IR. It also reduced renal tissue interleukin-1beta (IL-1 beta), interleukin-6 (IL-6), toll-like receptor-4 (TLR-4), phosphorylated-NF-kappa B, phosphorylated-I kappa B-alpha, tumor necrosis factor-alpha (TNF-alpha), and caspase-3 levels. In this study, TRPA1 antagonist HC-030031 showed a protective behavior on renal IR injury by averting inflammation and apoptosis. After further studies, TRPA1 inhibition may be a new treatment strategy to prevent renal IR injury.Öğe Protective Effects of TRPV1 Agonist Capsaicin in Sepsis-Induced Acute Kidney Injury in Rats(Wiley, 2025) Bircan, Burak; Cakir, Murat; Aydin, Ali; Firat, Semanur; Sekerci, Guldeniz; Samet, Oz; Tekin, SuatTransient receptor potential vanilloid-1 (TRPV1) channels have been shown to be present in many tissues, including the kidney. Previous studies have reported that TRPV1 activation has anti-inflammatory and renoprotective effects. In this study, we investigated the effects of TRPV1 agonist capsaicin on acute kidney injury (AKI) in a rat sepsis model induced by cecal ligation and puncture (CLP). Rats were divided into control, CLP and treatment groups in which 3 different doses of capsaicin (2, 6 and 30 mg/kg) were administered with CLP administration. Kidney tissues and sera from animals 24 h after CLP were analyzed. Histopathological examinations have shown that kidney damage occurs due to sepsis. TLR4/NF-kappa B activity, proinflammatory cytokines (IL-1 beta, IL-6, and TNF-alpha), caspase-3, caspase-8 and malondialdehyde levels increased in renal tissue due to sepsis. Serum levels of IL-1 beta, TNF-alpha and renal damage biomarkers (BUN, CRE, IL-18 and NGAL) increased due to sepsis. Capsaicin administration dose-dependently reversed sepsis-induced pathological changes in the kidney and serum. Our findings suggest that the TRPV1 agonist capsaicin has renoprotective effects in sepsis-induced AKI by reducing inflammation, oxidative damage and apoptosis. TRPV1 activation may be a promising therapeutic strategy to ameliorate sepsis-induced kidney and other organ damage.Öğe The ameliorative effect of inhibiting transient receptor potential ankyrin 1 on sepsis-induced kidney injury via the toll-like receptor 4/nuclear factor-kappa B pathway(Elsevier, 2025) Firat, Semanur; Cakir, Murat; Aydin, Ali; Bircan, Burak; Sekerci, Guldeniz; Tekin, SuatBackground Kidneys are among the organs most affected by sepsis caused by the host's uncontrolled immune response to infection. Transient receptor potential ankyrin 1 (TRPA1) channels have been shown to be associated with renal damage. TRPA1 channels also have a role in regulating intracellular Ca2+ levels, cytokine production, and immune response control. In this study, the effects of TRPA1 agonist ASP7663 and antagonist HC-030031 on renal injury in an experimental sepsis model were examined. Materials and methods Rats underwent cecal ligation and perforation (CLP) to serve as an experimental sepsis model. One of the two treatment groups received a TRPA1 agonist ASP7663, while the other received a TRPA1 antagonist HC030031. Serum levels of BUN, creatinine (Cre), TNF-alpha, IL-1 beta, IL-18, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) were measured. Histopathological examination of kidney tissue was performed. Immunohistochemical analysis of Toll-like receptor 4 (TLR4), NF-kappa B, phosphorylated NF-kappa B, I kappa B-alpha, phosphorylated I kappa B-alpha, TNF-alpha, IL-1 beta, IL-6, caspase-3, and caspase-8 levels was conducted in kidney tissue. Results CLP administration raised serum levels of BUN, Cre, TNF-alpha, IL-1 beta, IL-18, NGAL, and KIM-1 (P < 0.05). It also caused histopathological damage to kidney tissue. Additionally, CLP increased levels of TLR4, phosphorylated NF-kappa B, phosphorylated I kappa B-alpha, TNF-alpha, IL-1 beta, IL-6, caspase-3, and caspase-8 in kidney tissue (P < 0.05). The TRPA1 antagonist HC-030031 reversed all pathological changes in serum and kidney tissue caused by CLP. Conclusion TRPA1 antagonist HC-030031 showed a protective effect in an experimental sepsis model by reducing kidney damage through its anti-inflammatory and anti-apoptotic effects.Öğe The Effect of Sulfasalazine on Renal Damage in Sepsis Model Induced by Cecal Ligation and Puncture in Rats(Wiley, 2025) Cicek, Zeynep; Cakir, Murat; Aydin, Ali; Bircan, Burak; Firat, Semanur; Tekin, SuatSepsis is a medical condition that occurs when a harmful inflammatory response damages tissues and organs. The kidneys are among the organs most frequently affected by sepsis. Anti-inflammatory strategies are crucial in treating sepsis. The anti-inflammatory properties of sulphasalazine (SFZ) have been demonstrated in various in vitro and in vivo studies. This study investigates the effect of SFZ on kidney damage in a rat model of sepsis induced by the cecal ligation and puncture (CLP) method. Animals were divided into control, CLP, CLP + SFZ50, and CLP + SFZ250. Two doses of SFZ (50 and 250 mg/kg) were applied in two different treatment groups after CLP. The administration of SFZ reduced the CLP-induced increase in serum blood urea nitrogen (BUN), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), and creatinine (Cre) levels for both doses (p < 0.05). Additionally, SFZ treatment significantly decreased histopathological damage, phosphorylated NF-kappa B, toll-like receptor-4 (TLR-4), IL-1 beta, phosphorylated I kappa B-alpha, interleukin-6 (IL-6), TNF-alpha, caspase-3, and caspase-8 levels (p < 0.05). In this study, we found that two different doses of SFZ (50 and 250 mg/kg) showed protective effects by decreasing inflammation and kidney damage in a CLP-induced experimental sepsis model.
