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    Avanafil as a Novel Therapeutic Agent Against LPS-Induced Acute Lung Injury via Increasing CGMP to Downregulate the TLR4-NF-?B-NLRP3 Inflammasome Signaling Pathway
    (Springer, 2022) Aydin, Pelin; Magden, Zeynep Berna Aksakalli; Uzuncakmak, Sevgi Karabulut; Halici, Hamza; Akgun, Nurullah; Mendil, Ali Sefa; Mokhtare, Behzad
    Aim We demonstrate the effect of PDE5 inhibitors in cases of acute lung injury via the relationship between cGMP/NO and the TLR4-NF-kappa B-NLRP3 pathway. Materials and Methods This study was performed with 30 male Wistar albino rats. Lipopolysaccharide (LPS) was administered intratracheally to the rats and acute lung injury (ALI) was induced. Twelve hours after LPS administration, avanafil, prepared at suitable doses according to the body weights of the animals, was administered by oral gavage. Lung tissue samples of all groups were examined histopathologically and by immunochemical staining (IL-1 beta, iNOS, TLR4, and NF-kappa B). The iNOS, NLRP3, and IL-1B mRNA expression levels in the lung tissues were measured by RT-PCR. The left upper lobes of the rat lungs were dried at 70 degrees C for 48 h and lung water content was calculated. Result Statistically significant increases in iNOS, NLRP3, and IL-1 beta mRNA expressions were observed in the rats with ALI compared to the healthy controls (p < 0.0001). Those increased expressions were reduced at both doses of avanafil (p < 0.0001). This reduction was found to be greater at 20 mg/kg (p < 0.0001). IL-1 beta, iNOS, TLR4, and NF-kappa B immunopositivity was moderate/severe in the ALI group and mild in the group with ALI + avanafil at 20 mg/kg (p < 0.05). When the wet/dry lung ratios were calculated, a statistically significant increase was seen in the ALI group compared to the healthy rats (p < 0.05). That increase was decreased with both avanafil doses (p < 0.05). Conclusion We suggest that avanafil may prevent the progression of ALI and be effective in its treatment. We hope that this study will be supported by future clinical studies to yield a new indication for avanafil.
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    The melatonin agonist ramelteon attenuates bleomycin-induced lung fibrosis by suppressing the NLRP3/TGF-?1/HMGB1 signaling pathway
    (Elsevier Urban & Partner Sp Z O O, 2023) Aydin, Pelin; Aksakalli-Magden, Zeynep B.; Civelek, Maide S.; Karabulut-Uzuncakmak, Sevgi; Mokhtare, Behzad; Ozkaraca, Mustafa; Alper, Fatih
    Purpose: The possible effects of ramelteon, a melatonin receptor agonist on bleomycin-induced lung fibrosis were analyzed via transforming growth factor beta 1 (TGF-beta 1), the high mobility group box 1 (HMGB1) and Nod-like receptor pyrin domain-containing 3 (NLRP3) which are related to the fibrosis process. Materials and methods: Bleomycin (0.1 mL of 5 mg/kg) was administered by intratracheal instillation to induce pulmonary fibrosis (PF). Starting 24 h after bleomycin administration, a single dose of ramelteon was administered by oral gavage to the healthy groups, i.e. PF + RM2 (pulmonary fibrosis model with bleomycin + ramelteon at 2 mg/kg) and PF + RM4 (pulmonary fibrosis model with bleomycin + ramelteon at 4 mg/kg) at 2 and 4 mg/kg doses, respectively. Real-time polymerase chain reaction (real-time PCR) analyses, histopathological, and immunohistochemical staining were performed on lung tissues. Lung tomography images of the rats were also examined. Results: The levels of TGF-beta 1, HMGB1, NLRP3, and interleukin 1 beta (IL-1 beta) mRNA expressions increased as a result of PF and subsequently decreased with both ramelteon doses (p < 0.0001). Both doses of ramelteon partially ameliorated the reduction in the peribronchovascular thickening, ground-glass appearances, and reticulations, and the loss of lung volume. Conclusions: The severity of fibrosis decreased with ramelteon application. These effects of ramelteon may be associated with NLRP3 inflammation cascade.