Protective Effect of Hesperetin and Naringenin against Apoptosis in Ischemia/Reperfusion-Induced Retinal Injury in Rats

Purpose. Hesperetin and naringenin are naturally common flavonoids reported to have antioxidative effects. This study was performed to investigate whether either hesperetin or naringenin has a protective effect against apoptosis on retinal ischemia/reperfusion (I/R) injury. Methods. Retinal I/R was induced by increasing the intraocular pressure to 150 mmHg for 60 minutes. Thirty-three male Wistar albino rats were randomised into 5 groups named control, I/R + sham, I/R + solvent (DMSO), I/R + hesperetin, and I/R + naringenin. Animals were given either hesperetin, naringenin, or the solvent intraperitoneally immediately following reperfusion. Thickness of retinal layers and retinal cell apoptosis were detected by histological analysis, tunel assay, and immunohistochemistry assay. Results. Hesperetin and naringenin attenuated the I/R-induced apoptosis of retinal cells in the inner and outer nuclear cells of the rat retina. Retinal layer thickness of the naringenin treatment group was significantly thicker than that of the hesperetin, sham, and solvent groups (P<0.05). Conclusions. Hesperetin and naringenin can prevent harmful effects induced by I/R injury in the rat retina by inhibiting apoptosis of retinal cells, which suggests that those flavanones have a therapeutic potential for the protection of ocular ischemic diseases

Effect of Low-flow Anesthesia Education on Knowledge, Attitude and Behavior of the Anesthesia Team

AbstractThe aim of this study was to evaluate the effect of education on the knowledge, attitude and behavior of anesthesiology staff and residents towards low-flow anesthesia. The staff and residents in the Department of Anesthesia and Reanimation, Zonguldak Karaelmas University were given theoretical and practical training in delivering low-flow anesthesia. To evaluate their attitudes and behaviors toward low-flow anesthesia, we collected data during the 6 months before training, during the first 3 months after training, and at 4–6 months after training. Anesthesia follow-up records, operation time, volatile anesthetic agent used, and the amount (in liters) of fresh gas low mid-anesthesia were recorded in all three stages. A total of 3,158 patients received general anesthesia and inhalation anesthesia was used in 3,115 of these patients. Our study group consisted of 2,752 patients who had no absolute or relative contraindications to low-flow anesthesia. While the mean fresh gas flow was 4.00 ± 0.00 L/min before training, this level dropped to 2.98 L/min in the first 3 months after training, and to 3.26 L/min in the following 3 months. The mean fresh gas flow was significantly lower at the two post-training assessments than before training (p < 0.05). In conclusion, low-flow anesthesia may be used more frequently if educational seminars are provided to anesthetists. The use of low-flow anesthesia may increase further by allocating more time to this technique in anesthesia training programs provided at regular intervals

Effect of Coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats

<p>Abstract</p> <p>Background</p> <p>Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q₁₀(CoQ₁₀), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ₁₀in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ₁₀administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out.</p> <p>Results</p> <p>In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (<it>p </it>< 0.05). Administration of CoQ₁₀after trauma was shown to be protective because it significantly lowered the increased MDA levels (<it>p </it>< 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ₁₀group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ₁₀and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (<it>p </it>< 0.05).</p> <p>Conclusion</p> <p>Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ₁₀use in rats with traumatic brain injury.</p