RESUMEN
OBJECTIVE: Gastrodin, a glucoside of gastrodigenin, inhibits cerebral oxidant stress and apoptosis in multiple central nervous system injury, but its effect in intracerebral hemorrhage (ICH) remains unclear. This study investigated the effect of gastrodin on neuronal apoptosis and neurological deficits in rat ICH model. METHODS: In vitro experiments were performed using hematoma lysate-induced cell damage model in primary cortical neurons. Rat ICH model was produced by a caudatum injection of collagenase. Gastrodin was intraperitoneal injected after 2 hours following ICH. Cell viability, brain water content, neurological score, western blot, and immunofluorescence experiments were performed. RESULTS: Gastrodin significantly decreased hematoma lysate-induced reduction of cell viability and cell apoptosis in primary cortical neurons. Gastrodin significantly improved brain edema and neurological deficits post-ICH. Moreover, gastrodin administration significantly reduced levels of ROS, 8-OHDG, 3-Nitrotyrosine and MDA, while increased GSH-Px and SOD activity, and stimulated the upregulation of Keap1, Nrf2, and HO-1 signaling at 72 hours post-ICH. Furthermore, gastrodin significantly increased Bcl-2 expression, while reduced level of Bax, active caspase-3 and active caspase-9, also reduced the number of active caspase-3 or TUNEL positive neurons at 72 hours post-ICH. CONCLUSION: These results suggest that gastrodin is neuroprotective after ICH and the mechanism may be associated with the inhibition of oxidative stress and neuronal apoptosis.
Asunto(s)
Apoptosis/efectos de los fármacos , Alcoholes Bencílicos/farmacología , Corteza Cerebral/efectos de los fármacos , Hemorragia Cerebral/tratamiento farmacológico , Glucósidos/farmacología , Neuronas/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Animales , Proteínas Reguladoras de la Apoptosis/metabolismo , Conducta Animal/efectos de los fármacos , Edema Encefálico/metabolismo , Edema Encefálico/patología , Edema Encefálico/prevención & control , Células Cultivadas , Corteza Cerebral/metabolismo , Corteza Cerebral/patología , Corteza Cerebral/fisiopatología , Hemorragia Cerebral/metabolismo , Hemorragia Cerebral/patología , Hemorragia Cerebral/fisiopatología , Modelos Animales de Enfermedad , Masculino , Actividad Motora/efectos de los fármacos , Neuronas/metabolismo , Neuronas/patología , Estrés Oxidativo/efectos de los fármacos , Ratas Sprague-Dawley , Transducción de SeñalRESUMEN
BACKGROUND: Convulsive-like movements are rare in basilar artery occlusive cerebral infarction (BAOCI). These manifestations may easily be mistaken for epileptic seizures caused by compromised anterior circulation or by cortical lesions. Delayed diagnosis of this condition affects its subsequent treatment and prognosis. Therefore, it is critical to recognize this type of phenomenon in the early stage. CASE SUMMARY: A 55-year-old male patient presented with unconsciousness, rigidity, and a paroxysmal twitch in both lower limbs. These conditions lasted for nearly 2 h and resembled status epilepticus. After the initial conditions subsided, hemiplegia occurred and then subsided rapidly. The family refused thrombolytic therapy because the symptoms were similar to Todd paralysis after epilepsy. However, magnetic resonance imaging showed left pontine infarction. No abnormality was observed in a video electroencephalogram during the interictal period. Digital subtraction angiography revealed that the basilar artery was occluded and that the posterior communicating arteries were patent. Fortunately, the patient received a good prognosis after antiplatelet therapy, lipid regulation, balloon dilatation of the basilar artery, and rehabilitation. CONCLUSION: Convulsive-like movements may be an early sign of basilar artery occlusive brainstem infarction. It is important to identify this phenomenon in a timely manner.