Browsing by Author "Erol, Huseyin Serkan"

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(1 → 3)-β-d-glucan enhances the toxicity induced by Bortezomib in rat testis.
(2020-03-01T00:00:00Z) Akaras, Nurhan; Abuc, Ozlem Ozgul; Koc, Kubra; Bal, Tugba; Geyikoglu, Fatime; Atilay, Hilal; Erol, Huseyin Serkan; Yigit, Serdar; Gul, Murat
We aimed to determine the possible effects of the antioxidant agent (1 → 3)-β-D-glucan on bortezomib-induced rat testis damage. We used five groups of rats; control, (1 → 3)-β-D-glucan (75 mg/kg), bortezomib group, bortezomib + (1 → 3)-β-D-glucan groups (injection of (1 → 3)-β-D-glucan after bortezomib and sacrificed at 48th or 72nd h). The effects of these substances were assessed by measuring the levels of the antioxidant enzymes and LPO, and by performing immunohistochemical analysis with NF-κB. The histology of testis was evaluated using aniline blue staining. (1 → 3)-β-D-glucan leads to significant reductions in the levels of antioxidant enzymes and increased levels of LPO in testes. Moreover, it increased the NF-κB immunopositivity significantly in testis, especially in Bortezomib + (1 → 3)-β-D-glucan group at 48th h. The histological changes were observed in the bortezomib and/or (1 → 3)-β-D-glucan groups. Our results demonstrated that testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)-β-D-glucan and shockingly it increased the damage. PRACTICAL APPLICATIONS: The testis damage caused by the treatment with bortezomib was not eliminated by (1 → 3)-β-D-glucan and as a result, β-1,3-(D)-glucan enhanced the toxicity by leading a decrease in the levels of GSH, SOD, and CAT, thus caused an elevation in the immunoreactivity of NF-κB and altered the histopathological changes by enhancing the toxic effects of bortezomib. The findings of the previous studies about the antioxidative activity of (1 → 3)-β-D-glucan are controversial. So, it is necessary to consider the cytotoxicity of (1 → 3)-β-D-glucan in testis tissue. Thus, more studies on testis tissue are necessary to confirm that (1 → 3)-β-D-glucan is safe as an antioxidant.
Dietary effect of grape (Vitis vinifera) seed extract mitigates hepatic disorders caused by oxidized fish oil in rainbow trout (Oncorhynchus mykiss).
(2023-04-25T00:00:00Z) Terzi, Funda; Demirci, Beste; Acar, Ümit; Yüksel, Süleyman; Salum, Çağatay; Erol, Huseyin Serkan; Kesbiç, Osman Sabri
The major goal of this study was to determine the effect of grape seed extract (GSE) on liver damage in rainbow trout (Oncorhynchus mykiss) that was caused by the consumption of dietary oxidized fish oil (OFO). Rainbow trout were fed six different experimental diets coded OX-GSE 0 (OFO diet), OX-GSE 1 (OFO and 0.1% GSE), OX-GSE 3 (OFO and 0.3% GSE), GSE 0 (fresh fish oil and 0.0% GSE), GSE 1 (fresh fish oil and 0.1% GSE), and GSE 3 (fresh fish oil and 0.3% GSE) for 30 days. The lowest % hepatosomatic index (HSI) result was calculated in fish fed with OX-GSE 0 and the highest HSI was determined in fish fed with GSE 1 diets (p < 0.05). Histopathologically, hydropic degeneration in hepatocytes significantly increased OX-GSE 0 and GSE 3 compared to GSE 1 diets (p < 0.05). Deposition of lipid droplets in hepatocytes was significantly increased in OX-GSE 0 and OX-GSE 3 groups than others (p < 0.05). Liver biochemistry parameters such as superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) were significantly affected by OX and GSE treatments (p < 0.05). There were significant differences in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) among the liver enzymes analyzed in serum in OX and GSE (p < 0.05), meanwhile no difference was observed in lactate dehydrogenase (LDH) values between groups (p > 0.05). In conclusion, liver biochemistry and histopathology of rainbow trout consuming diets containing oxidized fish oil were negatively affected. However, it was determined that the supplementation of 0.1% GSE to the diet had a significant ameliorative role in these adverse effects.
Effects of tocilizumab and dexamethasone on the downregulation of proinflammatory cytokines and upregulation of antioxidants in the lungs in oleic acid-induced ARDS.
(2022-09-17T00:00:00Z) Terzi, Funda; Demirci, Beste; Çınar, İrfan; Alhilal, Mohammad; Erol, Huseyin Serkan
Acute respiratory distress syndrome (ARDS) is a life-threatening disease caused by the induction of inflammatory cytokines and chemokines in the lungs. There is a dearth of drug applications that can be used to prevent cytokine storms in ARDS treatment. This study was designed to investigate the effects of tocilizumab and dexamethasone on oxidative stress, antioxidant parameters, and cytokine storms in acute lung injury caused by oleic acid in rats.
Gossypin mitigates oxidative damage by downregulating the molecular signaling pathway in oleic acid-induced acute lung injury.
(2023-09-11) Dincer, Busra; Cinar, Irfan; Erol, Huseyin Serkan; Demirci, Beste; Terzi, Funda
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-α, IL-1β, 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.
Hispidulin exerts a protective effect against oleic acid induced-ARDS in the rat via inhibition of ACE activity and MAPK pathway.
(2023-01-09T00:00:00Z) Koc, Kubra; Ozek, Nihal Simsek; Aysin, Ferhunde; Demir, Ozlem; Yilmaz, Asli; Yilmaz, Mehmet; Geyikoglu, Fatime; Erol, Huseyin Serkan
This study investigates the protective role of Hispidulin on acute respiratory distress syndrome (ARDS) in rats. Rats were divided into three groups: control, ARDS, ARDS+ Hispidulin. The ARDS models were established by injecting rats with oleic acid. Hispidulin (100 mg/kg) was injected i.p. an hour before ARDS. Myeloperoxidase (MPO), Interleukin-8 (IL-8), Mitogen-activated protein kinases (MAPK), Lipid Peroxidation (LPO), Superoxide Dismutase (SOD), Glutathione (GSH), and Angiotensin-converting enzyme (ACE) were determined by ELISA. Tumor necrosis factor-alpha (TNF-α) expression was described by RT-qPCR. Caspase-3 immunostaining was performed to evaluate apoptosis. Compared with the model group, a significant decrease was observed in the MPO, IL-8, MAPK, ACE, LPO levels, and TNF-α expression in the ARDS+ Hispidulin group. Moreover, reduced caspase-3 immunoreactivity and activity of ACE were detected in the Hispidulin+ARDS group. The protective effect of Hispidulin treatment may act through inhibition of the ACE activity and then regulation of inflammatory cytokine level and alteration of apoptosis.
Protective effects of a natural product, paeoniflorin, on ischemia reperfusion injury on rat ovary tissue: histopathological, immunohistochemical, and biochemical study.
(2023-06-22T21:00:00Z) Bayram, Pinar; Karamese, Selina Aksak; Erol, Huseyin Serkan; Ozdemir, Bengul; Toktay, Erdem; Salum, Cagatay
In this study, the main hypothesis is that paeoniflorin may inhibit some cellular processes such as oxidative stress and inflammation. For this reason, we aimed to investigate the potential protective effects of a natural compound, paeoniflorin, on rat model of ovarian ischemia-reperfusion injury by detecting the oxidative stress parameters and inflammatory process parameters. 42 female Wistar-albino rats were divided into 6 random groups. The rats were subjected to 3-hour ischemia and 3-hour reperfusion process. Then, paeoniflorin at doses of 25, 50 and 100 mg/kg were applied 30 min before the reperfusion. The levels of pro-inflammatory (IL-1-β, IL-6, TNF-α) and anti-inflammatory (IL-10, TGF-β) cytokines were measured by ELISA. Similarly, IL-6, IL-10, TNF-α, NF-κB p65) positivity rates were detected by immunohistochemical staining. Additionally, oxidative stress parameters (MDA, GSH, SOD) were measured by tissue biochemistry. Ischemia-reperfusion injury caused significant increase in the levels of SOD, MDA, TNF-α, IL-1-β, IL-6 and NF-κB p65, while paeoniflorin treatments improved the related parameters in a dose-dependent manner. As a conclusion, our findings support the evidence that paeoniflorin has a potential protective effects on ovarian ischemia-reperfusion injury. Further detailed studies should be performed to shed light the molecular mechanism of these protective effects.
The Protection Potential of Antioxidant Vitamins Against Acute Respiratory Distress Syndrome: a Rat Trial.
(2019-10-01T00:00:00Z) Erol, Nazli; Saglam, Leyla; Saglam, Yavuz Selim; Erol, Huseyin Serkan; Altun, Serdar; Aktas, Mustafa Sinan; Halici, Mesut Bunyami
Acute respiratory distress syndrome (ARDS) is a fatal disease that includes inflammation formed by septic and non-septic causes. Reactive oxygen radicals (ROS) play a key role in ARDS pathophysiology and constitute the base of damage process. Antioxidant vitamins are used for inhibiting hazardous effects of radicals. Therefore, effects of antioxidant vitamins such as α-lipoic acid (ALA), vitamin E (VITE), and C (VITC) were investigated on oleic acid (OA)-induced ARDS rat model. Furthermore, high and low dose of methylprednisolone (HDMP, LDMP) was used for comparing effects of the vitamins. In this study, 42 male rats were divided to seven groups named control, OA, ALA, VITE, VITC, LDMP, and HDMP. OA was intravenously administered to all groups except control group and other compounds were orally administered (ALA, VITE, and VITC: 100 mg/kg, LDMP: 5 mg/kg, HDMP: 50 mg/kg) after OA injections. OA increased MDA level in lung tissue and TNF-α and IL-1β cytokine levels in serum. ALA, VITE, VITC, and both dose of MP significantly decreased the cytokine levels. Although OA reduced SOD, CAT, and GSH levels in lung tissue, the vitamins and LDMP markedly enhanced the levels except for HDMP. Furthermore, OA showed thickening in bronchi and alveolar septum, hyperemia in vessels, and inflammatory cell infiltrations in lung tissue histopathological examinations. Antioxidant vitamins may be useful for premedication of ARDS and similar disorders. However, methylprednisolone was not found sufficient for being a therapeutic agent for ARDS.
Two Flavonoids, Baicalein and Naringin, are Effective as Anti-Inflammatory and Anti-Oxidant Agents in a Rat Model of Polymicrobial Sepsis.
(2023-03-29T00:00:00Z) Bayram, Pinar; Aksak Karamese, Selina; Ozdemır, Bengul; Salum, Cagatay; Erol, Huseyin Serkan; Karamese, Murat
In this study, our aim was to investigate the possible protective and therapeutic effects of these two flavonoids, baicalein and naringin, in 50 and 100 mg/kg doses applied both before and after cecal ligation and puncture (CLP) procedures in a polymicrobial sepsis rat model, and evaluate possible contribution of oxidative and inflammatory markers by immunological, biochemical, molecular, and histopathological methods.