Browsing by Author "Erol H.S."

Now showing 1 - 12 of 12

(1 → 3)-β-d-glucan enhances the toxicity induced by Bortezomib in rat testis
(2020-03-01) Akaras N.; Abuc O.O.; Koc K.; Bal T.; Geyikoglu F.; Atilay H.; Erol H.S.; Yigit S.; Gul M.
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.
Anti-ulcerogenic effect of osajin on indomethacin-induced gastric damage in rats
(2020-01-01) Erol H.S.; Cakir A.; Koc M.; Yildirim S.; Halici M.
Ulcer is the most common undesirable result of using non-steroid anti-inflammatory drugs such as indomethacin. In the present study, osajin was experimentally used on indomethacin-induced gastric ulcer in rats. Osajin was purified from Maclura pomifera (Raf.) C. K. Schneid fruits by using the chromatographic methods. Thirty six rats were divided into six groups as follows: healthy (control), IND (indomethacin), RAN (ranitidine, 25 mg/kg), OSJ 100 (osajin, 100 mg/kg), OSJ 200 (200 mg/kg) and OSJ 400 (osajin, 400 mg/kg). Following a 24-h fasting, IND was administered to the treatment groups at a dose of 25 mg/kg. RAN and OSJ were given orally to rats following 5 min of IND administration. Then, gastric tissues were taken 6 h after the IND administration. Determination of the ulcer area, pathological evidence, and biochemical indices such as lipid peroxidation, superoxide dismutase, glutathione, and catalase were performed. IND generated diffuse ulcer areas, severe hyperaemia, oedema, necrotic epithelium, and mononuclear cell infiltration in the mucosa, and significantly increased lipid peroxidation while also decreasing the glutathione concentration, superoxide dismutase and catalase activities of the tissue. OSJ and RAN showed significant amelioration on ulcer area and biochemical indices. Therefore, OSJ may be potentially therapeutic for gastric ulcers.
Dietary effect of grape (Vitis vinifera) seed extract mitigates hepatic disorders caused by oxidized fish oil in rainbow trout (Oncorhynchus mykiss)
(2023-01-01) Terzi F.; Demirci B.; Acar Ü.; Yüksel S.; Salum Ç.; Erol H.S.; Kesbiç O.S.
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
(2022-12-01) Terzi F.; Demirci B.; Çınar İ.; Alhilal M.; Erol H.S.
Background: 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. Methods: Adult male rats were divided into five groups: the CN (healthy rats, n = 6), OA (oleic acid administration, n = 6), OA + TCZ-2 (oleic acid and tocilizumab at 2 mg/kg, n = 6), OA + TCZ-4 (oleic acid and tocilizumab at 4 mg/kg, n = 6), and OA + DEX-10 (oleic acid and dexamethasone at 10 mg/kg, n = 6) groups. All animals were euthanized after treatment for histopathological, immunohistochemical, biochemical, PCR, and SEM analyses. Results: Expressions of TNF-α, IL-1β, IL-6, and IL-8 cytokines in rats with acute lung injury induced by oleic acid were downregulated in the TCZ and DEX groups compared to the OA group (P < 0.05). The MDA level in lung tissues was statistically lower in the OA + TCZ-4 group compared to the OA group. It was further determined that SOD, GSH, and CAT levels were decreased in the OA group and increased in the TCZ and DEX groups (P < 0.05). Histopathological findings such as thickening of the alveoli, hyperemia, and peribronchial cell infiltration were found to be similar when lung tissues of the TCZ and DEX groups were compared to the control group. With SEM imaging of the lung tissues, it was found that the alveolar lining layer had become indistinct in the OA, OA + TCZ-2, and OA + TCZ-4 groups. Conclusions: In this model of acute lung injury caused by oleic acid, tocilizumab and dexamethasone were effective in preventing cytokine storms by downregulating the expression of proinflammatory cytokines including TNF-α, IL-1β, IL-6, and IL-8. Against the downregulation of antioxidant parameters such as SOD and GSH in the lung tissues caused by oleic acid, tocilizumab and dexamethasone upregulated them and showed protective effects against cell damage.
Evaluation of the roflumilast effect supplemented with linezolid in pleural empyema in rats caused by intrapleural staphylococcus aureus inoculation
(2020-01-01) Kerget B.; Araz Ö.; Kerget F.; Erol H.S.; Özmen S.; Halıcı Z.; Akgün M.
In addition to tube drains, pleural empyema is treated with antibiotics and anti-inflammatory drugs. We aimed to evaluate the anti-inflammatory activity of roflumilast combined with linezolid in a rat model of pleural empyema induced by Staphylococcus aureus. A total of 40 rats were divided into 7 groups: sham (n = 4), S. aureus inoculation (n = 6), S. aureus + 10 mg/kg linezolid (n = 6), S. aureus + 5 mg/kg roflumilast (n = 6), S. aureus + 10 mg/kg linezolid + 5 mg/kg roflumilast (n = 6), S. aureus + 10 mg/kg roflumilast (n = 6), and S. aureus + 10 mg/kg linezolid + 10 mg/kg roflumilast (n = 6). Animals were administered linezolid 1 h before and 12 h after inoculation with S. aureus. Roflumilast was administered orally as a single dose 30 min before inoculation with S. aureus. Compared to linezolid treatment alone, linezolid combined with 5 mg/kg roflumilast significantly improved TNF-α, IL-1β, vasodilation/congestion, and tissue/pleural polynuclear leukocyte (PNL) infiltration (p < 0.05). Linezolid combined with 10 mg/kg roflumilast also provided a significant improvement in TNF-α, IL-1β, IL-6, endothelin-1, vasodilation/congestion, mesothelial cell damage, lung tissue PNL, and pleural PNL compared to linezolid alone (p < 0.05). Due to its anti-inflammatory effects and significant impact on recovery, roflumilast can be used in conjunction with antibiotherapy for the treatment of pleural empyema.
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
Hispidulin exerts a protective effect against oleic acid induced-ARDS in the rat via inhibition of ACE activity and MAPK pathway
(2023-01-01) Koc K.; Ozek N.S.; Aysin F.; Demir O.; Yilmaz A.; Yilmaz M.; Geyikoglu F.; Erol H.S.
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.
Osajin from Maclura pomifera alleviates sepsis-induced liver injury in rats: biochemical, histopathological and immunohistochemical estimation
(2023-01-01) Alhilal M.; Erol H.S.; Yildirim S.; Cakir A.; Koc M.; Celebi D.; Halici M.B.
This paper aimed to examine the impact of flavonoid osajin (OSJ) on liver damage induced by sepsis. A total of 30 male rats were divided into 5 groups (Sham, sepsis, OSJ 150, OSJ 300 and reference). During sepsis, elevated lipid peroxidation (LPO) level and catalase activity (CAT) and decreased glutathione (GSH) level and superoxide dismutase (SOD) activity were observed in hepatic tissues of sepsis group in comparison with Sham group. A strong interleukin-33 and caspase-3 expressions were detected in hepatic tissues of sepsis group. On the contrary, OSJ administration to OSJ 300 group showed a significant decrease (P < 0.001) in LPO level (176±2.926) and significant increase (P < 0.001) in GSH level (10.586±0.083) and SOD activity (29.152±0.094) in comparison with sepsis group (185.777±1.735, 8.246±0.124, 24.307±0.379 respectively). In addition, the consumption of OSJ reduced expressions of interleukin-33 and caspase-3 and improved histopathological integrity. In conclusions, OSJ has hepatoprotective effect against sepsis-induced liver injury.
Protective effects of a natural product, paeoniflorin, on ischemia reperfusion injury on rat ovary tissue: histopathological, immunohistochemical, and biochemical study
(2023-01-01) Bayram P.; Karamese S.A.; Erol H.S.; Ozdemir B.; Toktay E.; Salum C.
The effect of 900-MHz radiofrequency electromagnetic fields during the adolescence on the histological structure of rat testis and its androgen and estrogen receptors localization
(2021-01-01) Gur F.M.; Keles A.I.; Erol H.S.; Guven C.; Taskin E.; Kaya H.; Gur H.E.; Odaci E.; Halici M.B.; Timurkaan S.
Background: Mobile phones as an electronic device which are emitting radiofrequency-electromagnetic field (RF-EMF). In this study was intend to determine the contingent effects of cell phone induced RF-EMF on testicular tissue in adolescence. Materials and Methods: Rats in the RF-EMF group were exposed to 900 MHz RF-EMF, while sham and control rats were not. After the completion of the test steps, the testicular tissues which were rapidly removed from the body of sacrificed rats were examined by using histopathological and biochemical methods. Testicular tissues cut to 5 μm thickness undergo routine histological procedures. Thus, histopathological evaluation will be completed. Malondialdehyde (MDA), glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) levels in testicular tissues were measured by biochemical methods to determine whether oxidative stress occurred or not. Results: Histopathologic findings were not observed in any of the studied groups. There was also no difference between the groups in terms of localization of androgen and estrogen receptors. The incidence of apoptotic index and TUNEL-positive cells was similar in all three groups. In the RF-EMF group, although the levels of MDA and CAT were significantly higher, GSH levels were lower than the other groups. There was no essential difference between the groups in terms of SOD level. Conclusions: The obtained results of this study showed that exposed to 900 MHz RF-EMF in adolescents caused oxidative stress in the testes, but testicular damage which is caused to oxidative stress is remained too low to be detected by histopathological methods in this study.
The Protection Potential of Antioxidant Vitamins Against Acute Respiratory Distress Syndrome: a Rat Trial
(2019-10-15) Erol N.; Saglam L.; Saglam Y.S.; Erol H.S.; Altun S.; Aktas M.S.; Halici M.B.
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
(2023-01-01) Bayram P.; Aksak Karamese S.; Ozdemir B.; Salum C.; Erol H.S.; Karamese M.
Introduction: 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 the possible contribution of oxidative and inflammatory markers by immunological, biochemical, molecular, and histopathological methods. Methods: Sixty-six Wistar albino rats were divided into 11 groups. The pro-inflammatory (TNF-alpha, IL-1-beta, and IL-6) and anti-inflammatory (TGF-beta and IL-10) cytokine levels were measured by ELISA technique. CD3, CD68, and nuclear factor kappa B positivity rates were detected by immunohistochemical methods. Oxidative stress parameters (MDA, SOD, and GSH) were measured by tissue biochemistry. Results: Sepsis caused a significant increase in all pro-inflammatory cytokine levels and MDA activity. Also, it led to an increase in the positivities of CD3, CD68, and NF-κB markers. However, especially pre-CLP doses of baicalein and naringin inhibited the inflammation process by suppressing pro-inflammatory and increasing anti-inflammatory cytokine levels, as well as regulating the oxidative stress process by normalizing the oxidant/anti-oxidant enzyme levels. Conclusion: Both pre- and post-application of baicalein and naringin are quite effective to prevent sepsis-caused cellular processes. This protective and therapeutic effects by baicalein and naringin in animals with sepsis seems to be originated from the high antioxidant capacity and inhibition of pro-inflammatory cytokine production. Thus, those natural agents may prove to be valuable protective agent against septic shock.