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    Evaluation of miRNAs Related with Nuclear Factor Kappa B Pathway in Lipopolysaccharide Induced Acute Respiratory Distress Syndrome
    (Cellular & Molecular Biology Research Center, 2020) Azizoglu, Mustafa; Ayaz, Lokman; Bayrak, Gulsen; Yilmaz, Banu Coskun; Birbicer, Handan; Doruk, Nurcan
    This study aimed to determine the expression of nuclear factor kappa B (NF-kappa B) pathway related miRNAs in experimental acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide (LPS) in rats, and to elucidate the underlying molecular mechanism. Twenty four sprague dawley rats were randomly divided into two groups; LPS (n = 12) and control (n = 12). Experimental ARDS was induced by intraperitoneal injection of E. coli LPS in LPS group. Intraperitoneal saline was administered in control group. Serum and lung samples were collected from both groups. Inununohistochemistry staining was performed for interleukin 1 beta (IL-beta), tumor necrosis factor alpha (TNF-alpha), CD 68, and caspase-3 in lung samples. Intensity of staining was scored as strong, moderate, weak, and no for evaluation of IL-1 beta and TNF-alpha. In addition, caspase-3 and CD68-positive stained cells were counted in sections. Expressions of 9 miRNAs were determined by quantitative real-time PCR in serum samples. IL-1 beta and TNF-alpha staining scores were significantly higher in the LPS group in comparison with the control group (P = 0.04 and P = 0.02, respectively). In addition, caspase-3 and CD68-positive stained cells were significantly higher in the LPS group (P = 0.02). Expressions of seven miRNAs were significantly changed in the LPS group in comparison with the control group. While six miRNAs (miR-7a-5p, miR-7b, miR9a-5p, miR-21-5p, miR-29a-3p, and miR-138-5p) were up regulated, only miR-124-3p was down regulated. This study suggests that these miRNAs may have a role in the pathogenesis of ARDS related to NF-kappa B. However, this relationship needs to be examined in new studies by evaluation of pathways and target genes.
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    Expression of ER stress markers (GRP78 and PERK) in experimental nephrotoxicity induced by cisplatin and gentamicin: roles of inflammatory response and oxidative stress
    (Springer, 2023) Metin, Tuba Ozcan; Bayrak, Gulsen; Yaman, Selma; Doganer, Adem; Yoldas, Atila; Eser, Nadire; Aykan, Duygun Altintas
    This study aimed to establish the relationship between two endoplasmic reticulum (ER) stress proteins, glucose-regulated protein 78 (GRP78/BiP) and PKR-like endoplasmic reticulum kinase (PERK), and oxidative stress markers in cisplatin (CIS)-induced and gentamicin (GEN)-induced nephrotoxicity. The study consisted of five groups: control (saline solution only), CIS D2 (2.5 mg/kg for 2 days), CIS D7 (2.5 mg/kg for 7 days), GEN D2 (160 mg/kg for 2 days), and GEN D7 (160 mg/kg for 7 days). All rats were sacrificed 24 h after the last injection for standard clinical chemistry, and ultrastructural and histological evaluation of the kidney. CIS and GEN increased blood urea nitrogen (BUN) and serum creatinine (Cr) levels, as well as total oxidant status (TOS), while decreasing total antioxidant status (TAS) level in CIS D7 and GEN D7 groups. Histopathological and ultrastructural findings were also consistent with renal tubular damage. In addition, expression of markers of renal inflammation (tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta)) and ER stress markers (GRP78 and PERK) was significantly increased in the kidney tissue of rats treated with CIS and GEN for 7 days. These findings suggest that CIS and GEN administration for 7 days aggravates nephrotoxicity through the enhancement of oxidative stress, inflammation, and ER stress-related markers. As a result, the recommended course of action is to utilize CIS and GEN as an immediate but brief induction therapy, stopping after 3 days and switching to other drugs instead.