大麻二酚在缺氧缺血性损伤中的神经保护作用:新生小鼠的治疗窗口。
摘要来源:
cns Neurol疾病药物靶标。 2016年9月27日。EPUB2016 9月27日。PMID: 27686886 27686886
agr agr agr(s) Ceprián,Laura Jimenez,M Ruth Pazos,JoseMartínez-Orgado 文章隶属关系:Nagat Mohammed
摘要:
目标: 以非精神上的大脑方法: 9-10天大的C57BL6小鼠受到HI侮辱(左颈动脉电凝后10%氧气持续90分钟)。然后,使用S.C.管理CBD 1 mg/kg或车辆15分钟或1、3、6、12、18或24小时之后的侮辱结束后。 Seven days later brain damage was assessed using T2W Magnetic Resonance Imaging scan (ipsilateral hemisphere volume loss, IVHL) and histological studies: Nissl staining (neuropathological score), TUNEL staining (apoptotic damage) and immunohistochemistry with glial fibrillary acidic protein (astrocyte viability) or ionized calcium binding adaptor molecule (microglial激活)。
结果: hi后,CBD高达18小时,而HI降低了IHVL和神经病理学评分60%,Tunel+ Count+ Count+ Count+ Count 90%,而星形胶质细胞损失为50%。此外,CBD削弱了小胶质细胞的HI诱导增加。但是IHVL, apoptosis or astrogliosis reduction.
CONCLUSION: CBD shows a TTW of 18 h when administered to HI newborn mice, which represents a broader TTW than reported for other neuroprotective treatments including hypothermia.