Biochemical and immunohistochemical examination of the effects of ephedrine in rat ovary tissue

Purpose: It was aimed to investigate the biochemical and immunohistochemical effects of ephedrine (EPH) in bilateral ovariectomized rats. Methods: Twenty-four Sprague Dawley female rats were divided into three groups: control group: The abdomen was opened and closed without any treatment; ischemia-reperfusion (IR) group: 2 h of ischemia followed by 2 h of reperfusion were allowed to cause IR injury; IR+EPH group: oral EPH solution (5 mg/kg) was administered for 28 days. Results: Biochemical parameters were statistically significant in group comparisons. Increased interleukin-6 (IL-6) expression, degenerative preantral and antral follicle cells and inflammatory cells around blood vessels were seen in IR group. Negative IL-6 expression was observed in seminal epithelial cells, preantral and antral follicle cells in IR+EPH group. While caspase-3 activity increased in granulosa cells and stromal cells in IR group, caspase-3 expression was negative in preantral and antral follicle cells in the germinal epithelium and cortex in IR+EPH group. Conclusion: The effect of apoptosis, which occurs with the signaling that starts in the cell nucleus, caused the cessation of the stimulating effect at the nuclear level after EPH administration, and a decrease in the antioxidative effect in IR damage and inflammation in the apoptotic process.

The protection effect and mechanism of hyperbaric oxygen therapy in rat brain with traumatic injury

Abstract Purpose: To investigate the effect of hyperbaric oxygen therapy (HBOT) on traumatic brain injury (TBI) outcome. Methods: The modified Marmarou's weight drop device was used to generate non-lethal moderate TBI rat model, and further developed in vitro astrocytes culturing system. Then, we analyzed the expression changes of interested genes and protein by quantitative PCR and western blot. Results: Multiple HBO treatments significantly reduced the expression of apoptosis promoting genes, such as c-fos, c-jun, Bax and weakened the activation of Caspase-3 in model rats. On the contrary, HBOT alleviated the decrease of anti-apoptosis gene Bcl-2 and promoted the expression of neurotrophic factors (NTFs), such as NGF, BDNF, GDNF and NT-3 in vivo. As a consequent, the neuropathogenesis was remarkably relied with HBOT. Astrocytes from TBI brain or those cultured with 21% O2 density expressed higher NTFs than that of corresponding controls, from sham brain and cultured with 7% O2, respectively. The NTFs expression was the highest in astrocytes form TBI brain and cultured with 21% O2, suggesting a synergistic effect existed between TBI and the following HBO treatment in astrocytes. Conclusion: Our findings provided evidence for the clinical usage of HBO treating brain damages.

Neuroprotección por ácido valproico y cambios en la expresión de Bcl-2 y caspasa-3 activada en ratas sometidas a isquemia/reperfusión / Neuroprotective action of valproic acid accompanied of the modification on the expression of Bcl-2 and activated caspase-3 in the brain of rats submitted to ischemia/reperfusion

El ácido valproico, que además de ser un conocido antiepiléptico, una serie de trabajos en los últimos años lo proponen como un agente neuroprotector. En éste trabajo se investigó primeramente, si el ácido valproico protege a las neuronas del daño producido por el estrés oxidativo inducido por la isquemia-reperfusión en el cerebro de ratas sanas sometidas a la oclusión transitoria de la arteria cerebral media derecha; en segundo lugar, se indagó si este fármaco induce cambios en la expresión de Bcl-2 y caspasa 3-activada como un posible mecanismo de acción sobre la muerte celular del tipo apoptótico. La evaluación neurológica de los animales que fueron sometidos a isquemia/reperfusión y recibieron ácido valproico fue mejor que los que no lo recibieron. Por otro lado, los niveles de malondialdehído en el hemisferio cerebral derecho en las ratas tratadas con ácido valproico fueron inferiores a los del mismo hemisferio del grupo control, mientras la cantidad de proteínas carboniladas se redujeron un 67% en comparación al grupo control. Además, se encontró por western blot, que en homogeneizados de tejido cerebral de los animales sometidos a isquemia/reperfusión y que recibieron ácido valproico, hubo un aumento significativo de la densidad de las bandas correspondientes a Bcl-2 y una disminución de caspasa 3-activada en comparación a los que no fueron tratados con este fármaco. Se concluye que el tratamiento con ácido valproico previno el déficit neurológico en ratas sanas sometidas a isquemia-reperfusión, bloqueando el efecto de los radicales libres sobre lípidos y proteínas de la corteza cerebral afectada y se sugiere que posiblemente este fármaco interviene en la muerte por apoptosis inducida durante este tipo de lesión, pudiendo ser una alternativa terapéutica en el tratamiento de la isquemia cerebral.

Valproic acid, apart from being known as an anti-epileptic drug, has been proposed in the past few years, as a neuroprotective agent. The purpose of this study was to investigate firstly, if valproic acid protects the neurons from the damage produced by oxidative stress induced by ischemia-reperfusion in the brain of healthy rats, under the transitory occlusion of the right middle cerebral artery. Secondly it was studied if this antiepileptic drug induces changes on the expression of Bcl-2 and activated caspase-3 as a possible mechanism of action on apoptosis. The neurological evaluation of the animals that were subject to ischemia-reperfusion and received valproic acid was better than the ones who didn’t receive it. On another subject, the levels of malondialdehyde on the right cerebral hemisphere in the rats treated with valproic acid were below the levels of the control group in the same hemisphere, whereas the amount of carbonylated proteins was reduced by 67% compared to the control group. Besides, it was found by western blot, that in homogenized brain tissue of the animals under ischemia-reperfusion which received valproic acid, there was a rise on the density of the bands corresponding to Bcl-2, and a reduction of activated 3-capase in comparison to the ones who were not treated with the antiepileptic drug. It’s concluded that the treatment with valproic acid prevented the neurological deficit in healthy rats under Ischemia-reperfusion, blocking the effect of free radicals on lipids and proteins of the affected brain cortex, and it is suggested that the same drug intervenes on apoptosis induced during this type of damage, being able to be a therapeutic alternative in the treatment of cerebral ischemia.