Browsing by Author "Dincer, B."

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Gossypin mitigates oxidative damage by downregulating the molecular signaling pathway in oleic acid-induced acute lung injury
(2023.01.01) Dincer, B.; Cinar, I.; Erol, H.S.; Demirci, B.; Terzi, F.
One of the leading causes of acute lung injury, which is linked to a high death rate, is pulmonary fat embolism. Increases in proinflammatory cytokines and the production of free radicals are related to the pathophysiology of acute lung injury. Antioxidants that scavenge free radicals play a protective role against acute lung injury. Gossypin has been proven to have antioxidant, antimicrobial, and anti-inflammatory properties. In this study, we compared the role of Gossypin with the therapeutically used drug Dexamethasone in the acute lung injury model caused by oleic acid in rats. Thirty rats were divided into five groups; Sham, Oleic acid model, Oleic acid+Dexamethasone (0.1 mg/kg), Oleic acid +Gossypin (10 and 20 mg/kg). Two hours after pretreatment with Dexamethasone or Gossypin, the acute lung injury model was created by injecting 1 g/kg oleic acid into the femoral vein. Three hours following the oleic acid injection, rats were decapitated. Lung tissues were extracted for histological, immunohistochemical, biochemical, PCR, and SEM imaging assessment. The oleic acid injection caused an increase in lipid peroxidation and catalase activity, pathological changes in lung tissue, decreased superoxide dismutase activity, and glutathione level, and increased TNF-alpha, IL-1 ss, IL-6, and IL-8 expression. However, these changes were attenuated after treatment with Gossypin and Dexamethasone. By reducing the expression of proinflammatory cytokines and attenuating oxidative stress, Gossypin pretreatment provides a new target that is equally effective as dexamethasone in the treatment of oleic acid-induced acute lung injury.
Otoprotective Mechanisms of Carvone As An Antioxidant Agent Against Ototoxic Damage Caused By Paclitaxel
(2023.01.01) Dincer, B.; Atalay, F.; Tatar, A.
Objective: Ototoxicity is cellular damage caused by the use of solid treatments as chemotherapeutics in critical illnesses like cancer. The generation of free radicals is linked to fluctuating hearing loss caused by chemotherapeutics. Antioxidants can help to prevent ototoxicity-related oxidative damage. Carvone (CVN) is a monoterpene with excellent antioxidant properties that protect against oxidative damage. This study investigates the biochemical and functional aspects of CVN's putative otoprotective mechanisms against paclitaxel (PCX)-induced ototoxicity. Methods: 24 Wistar albino rats were assigned into four different groups: Control, CVN, PCX, and PCX+CVN. Once a week, the control group received saline. The PCX group received 5 mg/kg PCX intraperitoneally once a week (4 times). Once a week, the CVN group received 50 mg/kg intraperitoneally. The PCX+ CVN group received 5 mg/kg PCX followed by 5 mg/kg CVN once a week. All animals were subjected to deterioration product otoacoustic emission testing before (day 0) and after drug administration (day 23). Results: PCX showed an ototoxic effect by weakening otoacoustic emission values. PCX leads to significant otoacoustic emission value shifts ameliorated by CVN co-treatment (for 2000Hz p< .001, for 4000 levels p< .01, for 6000Hz p< .001, and for 8000 Hz p< .01 in PCX+CVN group). Furthermore, the PCX group had significantly greater malondialdehyde levels and significantly lower glutathione levels in the cochlear tissues, compared to the other groups. Co-administered CVN with PCX reversed these effects, making oxidative stress parameters close to those of the control group (for GSH levels p< .001, for MDA levels p< .01 in the PCX+CVN group). Conclusion: According to the findings, CVN appears to preserve cochlear function in rats against the disruptive effects of PCX.
Unlocking Synergistic Potential: Agomelatine Enhances the Chemotherapeutic Effect of Paclitaxel in Breast Cancer Cell Through MT1 Melatonin Receptors and ER-alpha Axis
(2023.01.01) Dincer, B.; Yildiztekin, G.; Cinar, I.
This study investigates the potential of agomelatine (AGO), a synthetic melatoninergic drug, in combination with paclitaxel (PTX) for the treatment of breast cancer. The effects of AGO, PTX and melatonin (MTN) on breast cancer cell viability were investigated, focusing on the role of MT1 receptors. Cell viability and gene expression were analyzed in MCF-7 and MDA-MB-231 breast cancer cell experiments. The results show that AGO has cytotoxic effects on breast cancer cells similar to MTN. Combining AGO and MTN with PTX showed synergistic effects in MCF-7 cells. The study also reveals differences in the molecular mechanisms of breast cancer between estrogen-positive MCF-7 cells and estrogen-negative MDA-MB-231 cells. Combination with AGO and PTX affects apoptosis-associated proteins in both cell types. The findings suggest that AGO, combined with PTX, may be a promising adjuvant therapy for breast cancer and highlight the importance of MTN receptors in its mechanism of action.