Electron Microscopic and Immunohistochemical Examination of the Effect of 2-Aminoethoxydiphenyl Borate on Optic Nerve Injury in A Rat Model.

OBJECTIVE: We conducted this study to explore the possible protective effect of 2-aminoethoxydiphenyl borate (2-APB) on experimentally induced optic nerve injury in an acute ischemia-reperfusion (AIR) model. MATERIALS AND METHODS: A total of 30 Wistar albino rats were randomly divided into sham, AIR, and AIR+treatment (AIR10) groups. In the sham group, AIR model was not created. In the AIR group, AIR model was created without the administration of drug. In the AIR10 group, 2-APB was administered 10 min before reperfusion. RESULTS: Tissue samples were subjected to histological, immunohistochemical, and electron microscopic procedures. Histopathological examination revealed intense hypertrophic cells, more glial cells, capillary dilatation, and intense demyelination areas in the AIR group compared to those in the sham and AIR10 groups. Immunohistochemical staining demonstrated an increase in Orai1 and STIM1 immunoreactivity in the AIR group but less intense staining in the AIR10 group. Electron microscopy revealed injury in optic nerve axons in the AIR group, whereas this type of injury occurred to a lesser extent in the AIR10 group. CONCLUSION: In rats, store-operated Ca2+ entry in the cell had an essential role in optic nerve ischemia-reperfusion injury, and 2-ABP may have a protective effect on optic nerve injury caused due to AIR.

(1 → 3)-ß-d-glucan enhances the toxicity induced by Bortezomib in rat testis.

We aimed to determine the possible effects of the antioxidant agent (1 â†’ 3)-ß-D-glucan on bortezomib-induced rat testis damage. We used five groups of rats; control, (1 â†’ 3)-ß-D-glucan (75 mg/kg), bortezomib group, bortezomib + (1 â†’ 3)-ß-D-glucan groups (injection of (1 â†’ 3)-ß-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 â†’ 3)-ß-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 â†’ 3)-ß-D-glucan group at 48th h. The histological changes were observed in the bortezomib and/or (1 â†’ 3)-ß-D-glucan groups. Our results demonstrated that testis damage caused by the treatment with bortezomib was not eliminated by (1 â†’ 3)-ß-D-glucan and shockingly it increased the damage. PRACTICAL APPLICATIONS: The testis damage caused by the treatment with bortezomib was not eliminated by (1 â†’ 3)-ß-D-glucan and as a result, ß-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 â†’ 3)-ß-D-glucan are controversial. So, it is necessary to consider the cytotoxicity of (1 â†’ 3)-ß-D-glucan in testis tissue. Thus, more studies on testis tissue are necessary to confirm that (1 â†’ 3)-ß-D-glucan is safe as an antioxidant.

Protective effects of beta glucan in brain tissues of post-menopausal rats: a histochemical and ultra-structural study.

Decline of estrogen during menopause has been associated with numerous significant changes that have been linked to many pathophysiological complications. In addition, ovarian hormone deficiency increases the production of reactive oxygen radicals which could result in oxidative stress and cell damage. While estrogen therapy is often considered to overcome the behavioral and physiological shortcomings, antioxidants are gaining popularity for their beneficial property. For this purpose, in the present study, utilizing the antioxidant properties of beta glucan has been examined in treatment of menopause induced oxidative stress in cerebral neurons. Four groups of female Wistar rats were used: control, ovariectomy, ovariectomy + estrogen treated and ovariectomy + beta glucan treated. We observed a significant increase in neural degeneration in ovariectomized rats as compared to controls. Moreover, increased oxidative stress in the brains of the ovariectomized rats has been detected by performing immunohistochemical analysis. A large number of immuno-positive cerebral neurons have been observed in ovariectomy group rat brains. Interestingly, providing beta glucan treatment to ovariectomized rats reduced the number of degenerated neurons. Our study is the first to examine light and electron microscopic examination and immunohistochemical and stereological analysis of estrogen depletion in rats and to test protective role of beta glucan in the experimental study.