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目的 探讨和厚朴酚对脑出血（intracerebral hemorrhage，ICH）小鼠神经损伤和认知功能的影响及其作用机制。 方法 将C57BL/6J小鼠随机分为假手术组，模型组，和厚朴酚低、中、高剂量组，以及和厚朴酚+抑制剂组。除假手术组外，其余组小鼠均通过自体血注入右侧基底神经节构建ICH模型。于ICH前15 min和ICH后1 h，和厚朴酚低、中、高剂量组分别腹腔注射10 mg/kg、20 mg/kg、40 mg/kg和厚朴酚，和厚朴酚+抑制剂组腹腔注射40 mg/kg和厚朴酚与5 μg/kg脑源性神经营养因子（brain derived neurotrophic factor，BDNF）-酪氨酸激酶受体B（tyrosine kinase receptor B，TrkB）-环磷酸腺苷反应元件结合蛋白（cyclic adenosine monophosphate response element binding protein，CREB）信号通路抑制剂K252a，假手术组、模型组腹腔注射等量的二甲基亚砜和生理盐水。采用改良的神经功能缺损评分（modified neurological severity score，mNSS）评估小鼠神经功能；通过Morris水迷宫实验计算逃避潜伏期、跨越原平台次数、目标象限停留时间百分比3个指标用于评估小鼠空间学习和记忆能力；苏木精-伊红（hematoxylin-eosin，HE）染色观察海马神经元病理学改变；原位末端转移酶标记（terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling，TUNEL）染色检测海马神经元凋亡率；酶联免疫吸附试验（enzyme-linked immunosorbent assay，ELISA）检测血清BDNF、TrkB水平；免疫印迹法检测海马组织BDNF、TrkB、CREB、磷酸化CREB（phosphorylated CREB，p-CREB）蛋白表达情况。 结果 与假手术组小鼠相比，模型组小鼠mNSS、海马神经元凋亡率升高，逃避潜伏期延长，跨越原平台次数减少，目标象限停留时间百分比降低，血清BDNF、TrkB及海马组织BDNF、TrkB、p-CREB/CREB水平降低（均P

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