The efficacy of hesperidin for treatment of acute otitis media.

OBJECTIVES: In this experimental study, the effect of hesperidin on the treatment of acute otitis media (AOM) was investigated in an AOM-induced rat model. METHODS: In total, 35 rats were randomly divided into the following five groups (n=7): group 1 (control), group 2 (AOM with no treatment), group 3 (AOM+antibiotic), group 4 (AOM+hesperidin), and group 5 (AOM+hesperidin+antibiotic). On day 14, group 3,4 and 5 rats were given antibiotic and hesperidin via gavages, respectively. Histopathological and immunological analyses were performed and the results analyzed. RESULTS: Serum levels of TNF-α, IL-4, IL-6 and IL-1ß were significantly decreased in the hesperidin- and antibiotic-treated groups compared to the AOM group. The AOM+antibiotic and AOM+hesperidin groups demonstrated reduced histological damage compared to the AOM group. Between the AOM+antibiotic and AOM+hesperidin groups, significant differences in tympanic membrane thickness(ThicTM), inflammation(Inf), and sclerosis(Sc) values were observed. However, no difference in epithelial damage(DamEpith), was seen between the two groups. There was a significant difference in the AOM+antibiotic and AOM+antibiotic+hesperidin groups compared to AOM group (P<0.001). CONCLUSIONS: In this study, we observed that both antibiotic and hesperidin treatment reduced AOM symptoms in an AOM-induced rat model. The values in AOM+antibiotic+hesperidin group were markedly lower than those of the other groups. From our results, we propose that hesperidin, in combination with antibiotics, may provide a successful alternative treatment for AOM compared with antibiotics used alone.

Neuroprotective effects of ß-myrcene following global cerebral ischemia/reperfusion-mediated oxidative and neuronal damage in a C57BL/J6 mouse.

The aim of this study was to investigate the effects of ß-myrcene (MYR) on oxidative and histological damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. Mice (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) MYR, and (4) MYR + I/R. The SH group was used as a control and received 0.1 % carboxymethyl cellulose (CMC) as a vehicle following a medial incision without carotid occlusion. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and treated with the vehicle intraperitoneally (i.p.) for 10 days. In the MYR group, mice were given 200 mg/kg MYR dissolved in 0.1 % CMC for 10 days following a medial incision without carotid occlusion. In the MYR + I/R group, the I/R procedure was performed exactly as in the I/R group, and they were then treated with the same dose of MYR for 10 days. Cerebral I/R induced oxidative stress via an increase in thiobarbituric acid reactive substances (TBARS) formation and a decrease in the antioxidant defense systems, including glutathione (GSH), catalase, glutathione peroxidase (GPx) and superoxide dismutase (SOD). However, MYR treatment protected against the oxidative effects of I/R by inducing significant increases in GSH, GPx, and SOD and a significant decrease in the formation of TBARS. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by MYR treatment. This study has demonstrated that MYR effectively attenuates oxidative and histological damage in the brain caused by global I/R. The beneficial effects of MYR probably contribute to its strong antioxidant and radical scavenging properties. In conclusion, MYR may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, may be a viable and safe alternative treatment for ischemic stroke in humans.

Hesperidin attenuates oxidative and neuronal damage caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.

The aim of this study was to determine the effects of hesperidin (HP) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. For this purpose, a total of 40 mice were divided equally into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) HP, and (4) HP+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with vehicle for 10 days. In the HP group, mice were administered HP (100 mg/kg) for 10 days without carotid occlusion. In the HP+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with 100 mg/kg HP for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidation and a decrease in the components of the antioxidant defense system. Furthermore, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue. HP treatment significantly reversed the oxidative effects of I/R and inhibited the development of neurodegenerative histopathology. Therefore, the current study demonstrates that HP treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, the beneficial effects of HP are likely a result of its strong antioxidant and free radical-scavenging properties. HP may be an useful treatment to attenuate the negative effects of global cerebral I/R.

The beneficial effects of 18ß-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model.

This study investigated the effects of 18ß-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.