Browsing by Author "Geyikoglu F."

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(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.
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.