中文摘要：

本文旨在探讨脑淋巴引流系统在蛛网膜下腔出血（subarachnoid hemorrhage，SAH）后神经元损伤中的作用。分别建立兔SAH、SAH＋脑淋巴引流阻滞（cerebral lymphatic blockage，CLB）模型，于SAH模型建立后5d抽取脑脊液，加入培养的大鼠海马神经元中，随机将神经元分为空白对照组、正常脑脊液组、SAH组、SAH＋CLB组，分别于培养0．5h、1h、2h、4h后，检测乳酸脱氢酶（1actate dehydrogenase，LDH）漏出率，流式细胞术检测神经元凋亡，免疫组织化学法检测细胞凋亡蛋白Bax、Hsp70的表达。结果显示：正常脑脊液对神经元LDH漏出率无影响，SAH组和SAH＋CLB组脑脊液使神经元LDH漏出率增加，以SAH＋CLB组更为显著；正常脑脊液没有引起神经元凋亡，SAH组出现神经元凋亡，SAH＋CLB组神经元凋亡更为严重。在SAH组和SAH＋CLB组均检测到Bax及Hsp70蛋白表达；Bax蛋白表达在SAH＋CLB组大于SAH组，且呈时间依赖性增强；在0．5h和1h，SAH＋CLB组Hsp70蛋白表达高于SAH组，而在2h和4h则表达减弱，SAH＋CLB组表达高峰（1h）早于SAH组（2h）。以上结果表明，CLB加重SAH脑脊液对神经元的损伤，提示脑淋巴引流系统在SAH后可能起到一定的内源性保护作用。

英文摘要：

This work was performed to determine the role of cerebral lymphatic drainage pathway in the development of neural injury following subarachnoid hemorrhage （SAH）. SAH and cerebral lymphatic blockage （CLB） models in adult New Zealand rabbits were used. Cerebrospinal fluid （CSF） was obtained from experimental animals 5 d after modeling and was added into cultured rat hippocam- pal neurons. The neurons were randomly divided into blank control, normal CSF, SAH, and SAH＋CLB groups. At different points of time, lactate dehydrogenase （LDH） leakage was detected by colorimetric method. Flow cytometry was used to detect the apoptosis of neurons. Expressions of Bax and heat-shock protein 70 （Hsp70） were determined by immunohistochemical staining. LDH leakage detection revealed that, compared with blank control group, CSF from normal rabbit did not damage the neurons, whereas the leakage of LDH increased in SAH group and SAH＋CLB group. The increasing effect was more obvious in SAH＋CLB group than that in SAH group. Normal CSF did not induce the apoptosis of neurons, whereas neuron apoptosis was found in SAH group and the apoptosis was even more severe in SAH＋CLB group. Bax and Hsp70 protein expressions were found in both SAH and SAH＋CLB groups. Expression of Bax protein in SAH＋CLB group was stronger than that in SAH group in a time-dependent manner. At 0.5 h and 1 h, the expression of Hsp70 protein in SAH＋CLB group was stronger than that in SAH group, whereas the expression became weaker at 2 h and 4 h. These results suggest that blockage of cerebral lymphatic drainage pathway deteriorates the damage of neurons treated with CSF from SAH, indicating this pathway may act as an endogenous protective role in SAH.