Browsing by Author "Dincer B."

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Antipsychotics Induced Reproductive Toxicity by Stimulating Oxidative Stress: A Comparative in Vivo and in Silico Study
(2023-01-01) Dincer B.; Bulent Yazici A.; Cinar I.; Toktay E.; Selli J.; Cadirci E.; Bayraktutan Z.; Yazici E.
The pathophysiological mechanism behind the link between antipsychotic drugs and sexual dysfunction is still unknown. The goal of this research is to compare the potential effects of antipsychotics on the male reproductive system. Fifty rats were randomly assigned into the five groups indicated: Control, Haloperidol, Risperidone, Quetiapine and Aripiprazole. Sperm parameters were significantly impaired in all antipsychotics-treated groups. Haloperidol and Risperidone significantly decreased the level of testosterone. All antipsychotics had significantly reduced inhibin B level. A significant reduction was observed in SOD activity in all antipsychotics-treated groups. While GSH levels diminished, MDA levels were rising in the Haloperidol and Risperidone groups. Also, the GSH level was significantly elevated in the Quetiapine and Aripiprazole groups. By causing oxidative stress and altering hormone levels, Haloperidol and Risperidone are damaging to male reproductivity. This study represents useful starting point for exploring further aspects of the underlying mechanisms reproductive toxicity of antipsychotics.
Does daily fasting shielding kidney on hyperglycemia-related inflammatory cytokine via TNF-α, NLRP3, TGF-β1 and VCAM-1 mRNA expression
(2021-11-01) Bilen A.; Calik I.; Yayla M.; Dincer B.; Tavaci T.; Cinar I.; Bilen H.; Cadirci E.; Halici Z.; Mercantepe F.
This study aimed to investigate the effects of blood glucose control and the kidneys' functions, depending on fasting, in the streptozotocin-induced diabetes model in rats via TNF-α, NLRP-3, TGF-β1 and VCAM-1 mRNA expression in the present study. 32 Wistar albino rats were allocated randomly into four main groups; H (Healthy, n = 6), HF (Healthy fasting, n = 6), D (Diabetes, n = 10), DF (Diabetes and fasting, n = 10). Blood glucose and HbA1c levels significantly increased in the D group compared to the healthy ones (p < 0.05). However, the fasting period significantly improved blood glucose and HbA1c levels 14 days after STZ induced diabetes in rats compared to the D group. Similar findings we obtained for serum (BUN-creatinine) and urine samples (creatinine and urea levels). STZ induced high glucose levels significantly up-regulated TNF-α, NLRP-3, TGF-β1 and VCAM-1 mRNA expression and fasting significantly decreased these parameters when compared to diabetic rats. Histopathological staining also demonstrated the protective effects of fasting on diabetic kidney tissue. In conclusion, intermittent fasting regulated blood glucose level as well as decreasing harmful effects of diabetes on kidney tissue. The fasting period significantly decreased the hyperglycemia-related inflammatory cytokine damage on kidneys and also reduced apoptosis in favor of living organisms.
Evaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue
(2022-03-01) Dincer B.; Cinar I.; Yayla M.; Toktay E.
Aim: Ovarian ischemia–reperfusion (I/R) injury is a serious gynecological condition that affects women of reproductive age and reduces ovarian reserve. Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury. Methods: Thirty-three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham-operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion. Results: IL-1β, IL-6, TNF-α, NF-κB, and CASP-3 mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, NF-κB, TNF-α, IL-1β, and IL-6 expressions. GOS was also corrected by reducing the elevated expression of CASP-3 as apoptosis-change marker. Conclusion: These findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis.
Gossypin mitigates oxidative damage by downregulating the molecular signaling pathway in oleic acid-induced acute lung injury
(John Wiley and Sons Ltd, 2023) 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 pul-monary fat embolism. Increases in proinflammatory cytokines and the production of freeradicals are related to the pathophysiology of acute lung injury. Antioxidants that scav-enge free radicals play a protective role against acute lung injury. Gossypin has beenproven to have antioxidant, antimicrobial, and anti-inflammatory properties. In this study,we compared the role of Gossypin with the therapeutically used drug Dexamethasonein the acute lung injury model caused by oleic acid in rats. Thirty rats were divided intofive 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 orGossypin, the acute lung injury model was created by injecting 1 g/kg oleic acid into thefemoral vein. Three hours following the oleicacid injection, rats were decapitated. Lungtissues were extracted for histological, immunohistochemical, biochemical, PCR, andSEM imaging assessment. The oleic acid injection caused an increase in lipid peroxidationand catalase activity, pathological changes in lung tissue, decreased superoxide dismu-tase activity, and glutathione level, and increased TNF-α,IL-1β, IL-6, and IL-8 expression.However, these changes were attenuated after treatment with Gossypin and Dexameth-asone. By reducing the expression of proinflammatory cytokines and attenuating oxida-tive stress, Gossypin pretreatment provides a new target that is equally effective asdexamethasone in the treatment of oleic acid-induced acute lung injury
Unlocking Synergistic Potential: Agomelatine Enhances the Chemotherapeutic Effect of Paclitaxel in Breast Cancer Cell Through MT1 Melatonin Receptors and ER-alpha Axis
(John Wiley and Sons Inc, 2023) 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.
Zingiberene attenuates paclitaxel-induced ototoxicity by strengthening cochlear antioxidant defense system in vivo
(2023-01-01) Dincer B.; Atalay F.; Tatar A.
Paclitaxel is widely used in the treatment of many cancers. Paclitaxel-induced ototoxicity is related to the neurotoxic effects of paclitaxel on auditory peripheral neurons. Zingiberene has significant antitumor and antioxidant properties. This study aimed to determine whether zingiberene protects against the ototoxicity caused by paclitaxel. Twenty-four Wistar Albino rats were divided into four groups. The control group received 1 ml/kg saline on days 1, 7, 14, and 21. The paclitaxel group received 5 mg/kg paclitaxel on days 1, 7, 14, and 21. On days 1, 7, 14, and 21, the zingiberene group received 10mg/kg of zingiberene. Paclitaxel + zingiberene group first 5 mg/kg paclitaxel and 30 minutes later 10mg zingiberene on the 1st, 7th, 14th, and 21st days. A distortion product-evoked otoacoustic emission test (DPOAE) was performed before (day 0) and after (day 22) of the experiment. The pretreatment DPOAE values of the groups were not significantly different. On day 22, the DPOAE results in the paclitaxel group showed a considerable decline. Malondialdehyde levels were substantially higher, and glutathione levels were much lower in the paclitaxel group. The paclitaxel+zingiberene group displayed significantly higher DPOAE levels than the paclitaxel group. Compared to the paclitaxel group paclitaxel+zingiberene, glutathione levels were considerably higher, and malondialdehyde levels were significantly lower. The study findings provide the first evidence in the literature that zingiberene can prevent ototoxicity from paclitaxel-induced hearing loss by lowering the levels of oxidant parameters. It demonstrates that administering zingiberene and paclitaxel together may be a practical clinical approach to alleviate paclitaxel-induced ototoxicity.