Browsing by Author "Halici, Mesut Bunyami"

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Citation - WoS: 5
Citation - Scopus: 5
Medicinal Evaluation and Molecular Docking Study of Osajin as an Anti-Inflammatory, Antioxidant, and Antiapoptotic Agent Against Sepsis-Associated Acute Kidney Injury in Rats
(Taylor & Francis Ltd, 2024) Alhilal, Mohammad; Erol, Huseyin Serkan; Yildirim, Serkan; Cakir, Ahmet; Koc, Murat; Alhilal, Suzan; Halici, Mesut Bunyami
Despite efforts to find effective drugs for sepsis-associated acute kidney injury (SA-AKI), mortality rates in patients with SA-AKI have not decreased. Our study evaluated the protective effects of isoflavone osajin (OSJ) on SA-AKI in rats by targeting inflammation, oxidative stress, and apoptosis, which represent the cornerstones in the pathophysiological mechanism of SA-AKI. Polymicrobial sepsis was induced in rats via the cecal ligation and puncture (CLP) technique. Markers of oxidative stress were evaluated in kidney tissues using biochemical methods. The expression of interleukin-33 (IL-33), 8-hydroxydeoxyguanosine (8-OHdG), caspase-3, and kidney injury molecule-1 (KIM-1) was evaluated as indicators of inflammation, DNA damage, apoptosis, and SA-AKI respectively in the kidney tissues using immunohistochemical and immunofluorescent detection methods. The CLP technique significantly (p < 0.001) increased lipid peroxidation (LPO) levels and significantly (p < 0.001) decreased the activities of superoxide dismutase and catalase in kidney tissues. In the renal tissues, strong expression of IL-33, 8-OHdG, caspase-3, and KIM-1 was observed with severe degeneration and necrosis in the tubular epithelium and intense interstitial nephritis. In contrast, the administration of OSJ significantly (p < 0.001) reduced the level of LPO, markedly improved biomarkers of antioxidant status, decreased the levels of serum creatinine and urea, lowered the expression of IL-33, 8-OHdG, caspase-3, and KIM-1 and alleviated changes in renal histopathology. A promising binding score was found via a molecular docking investigation of the OSJ-binding mode with mouse IL-33 (PDB Code: 5VI4). Therefore, OSJ protects against SA-AKI by suppressing the IL-33/LPO/8-OHdG/caspase-3 pathway and improving the antioxidant system.
Citation - WoS: 10
Citation - Scopus: 9
Osajin from Maclura pomifera alleviates sepsis-induced liver injury in rats: biochemical, histopathological and immunohistochemical estimation
(Taylor & Francis Online, 2023) Alhilal, Mohammad; Huseyin Serkan Erol, Serkan Yildirim, Ahmet Cakir, Murat Koc, Demet Celebi, Mesut Bunyami Halici; Koc, Murat; Cakir, Ahmet; Erol, Huseyin Serkan; Celebi, Demet; Yildirim, Serkan; Halici, Mesut Bunyami
This paper aimed to examine the impact of flavonoid osajin (OSJ) on liver damage induced by sepsis. A total of 30 male rats were divided into 5 groups (Sham, sepsis, OSJ 150, OSJ 300 and reference). During sepsis, elevated lipid peroxidation (LPO) level and catalase activity (CAT) and decreased glutathione (GSH) level and superoxide dismutase (SOD) activity were observed in hepatic tissues of sepsis group in comparison with Sham group. A strong interleukin-33 and caspase-3 expressions were detected in hepatic tissues of sepsis group. On the contrary, OSJ administration to OSJ 300 group showed a significant decrease (P < 0.001) in LPO level (176±2.926) and significant increase (P < 0.001) in GSH level (10.586±0.083) and SOD activity (29.152±0.094) in comparison with sepsis group (185.777±1.735, 8.246±0.124, 24.307±0.379 respectively). In addition, the consumption of OSJ reduced expressions of interleukin-33 and caspase-3 and improved histopathological integrity. In conclusions, OSJ has hepatoprotective effect against sepsis-induced liver injury.
Protocatechuic Acid Mitigates Diazinon-Induced Lung Injury in Rats through Modulation of Oxidative Stress, Inflammatory, Keap-1/Nrf-2/HO-1 and ER Stress-Mediated Apoptotic Pathways
(Mashhad Univ Med Sciences, 2026) Can, Ismail; Bozkurt, Ilyas; Senocak, Esra Aktas; Karaarslan, Tuba; Alat, Omercan; Halici, Mesut Bunyami; Gur, Cihan
Objective(s): Diazinon (DZN), a widely used organophosphate pesticide, induces pulmonary toxicity through oxidative stress, inflammation, endoplasmic reticulum (ER) stress, and apoptosis. This study investigated the potential protective effects of protocatechuic acid (PCA) against DZN-induced lung injury in rats. Materials and Methods: Thirty-five adult rats were randomly assigned to five groups (n = 7): Control, DZN (20 mg/kg), PCA100 (100 mg/kg), DZN + PCA50, and DZN + PCA100. Lung tissues were evaluated histopathologically, and oxidative stress markers (GSH, SOD, CAT, and GPx) and inflammatory mediators (TNF-alpha, IL-1 beta, IL-6, NF-kappa B, COX-2, and iNOS) were measured by ELISA. The protein levels of Keap-1, Nrf2, and HO-1 were assessed via Western blotting. Expression of ER stress-related genes (XBP-1, eIF2, ATF4, CHOP) and apoptotic markers (Bax, Bcl-2, caspase-3, -6, -9) was analyzed by qRT-PCR. Results: DZN exposure caused severe histopathological damage and significantly increased oxidative, inflammatory, ER stress, and apoptotic responses. PCA administration, particularly at 100 mg/kg, markedly improved lung morphology, normalized antioxidant enzyme levels, reduced cytokine production and NF-kappa B activation, and downregulated ER stress and apoptosis-related genes. PCA also enhanced Bcl-2 expression and activated the Nrf2/HO-1 signaling pathway. Conclusion: PCA exerts dose-dependent protective effects against DZN-induced pulmonary toxicity by modulating oxidative stress, inflammation, ER stress, and apoptosis. These findings suggest that PCA may serve as a promising therapeutic candidate for mitigating pesticide-related lung injury.