1. Gastrodin Attenuates Neuronal Apoptosis and Neurological Deficits after Experimental Intracerebral Hemorrhage
- Author
-
Xiao-fei Hu, Xiao-ping Jin, En Wang, Chang-zhu Wu, Ting-ling Wang, Xi-chang Liu, Shao-fa Ke, and Gang Wu
- Subjects
Male ,Apoptosis ,Brain Edema ,Motor Activity ,Pharmacology ,medicine.disease_cause ,Neuroprotection ,Rats, Sprague-Dawley ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Glucosides ,Animals ,Medicine ,cardiovascular diseases ,Viability assay ,Gastrodin ,Cell damage ,Benzyl Alcohols ,Cells, Cultured ,Cerebral Hemorrhage ,Cerebral Cortex ,Neurons ,Intracerebral hemorrhage ,Behavior, Animal ,business.industry ,Rehabilitation ,medicine.disease ,Gastrodigenin ,Disease Models, Animal ,Oxidative Stress ,Neuroprotective Agents ,chemistry ,Surgery ,Neurology (clinical) ,Apoptosis Regulatory Proteins ,Cardiology and Cardiovascular Medicine ,business ,030217 neurology & neurosurgery ,Oxidative stress ,Signal Transduction - Abstract
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.
- Published
- 2020
- Full Text
- View/download PDF