目的：探讨梓醇对高糖损伤的血管内皮细胞（ECV-304）的影响。方法：体外培养ECV-304细胞，采用MTT法测定细胞的增殖，分光光度计法检测一氧化氮（NO）、乳酸脱氢酶（LDH）,观察梓醇对高糖损伤的ECV-304的影响。结果：各浓度组梓醇对糖含量正常培养液中培养的ECV-304细胞活力无明显改变。与空白组比较，高糖损伤模型组细胞活力明显下降（P<0.01）, NO释放显著减少（P<0.01）, LDH释放水平显著升高（P<0.01）；与高糖损伤模型组比较，低、中剂量组细胞活力和NO未见改变，但LDH水平下降（P<0.01）；与高糖模型组比较，高剂量梓醇组细胞活力明显增加（P<0.01）, NO释放增加（P<0.05），LDH水平明显下降（P<0.01）。结论：梓醇可能通过调节NO和LDH水平，实现对高糖诱导ECV-304的损伤保护效应。

This study was aimed to investigate the protective effect of catalpol against high glucose induced injury on vascular endothelial cells (ECV-304). ECV-304 cells were cultured in vitro. MTT method was applied to detect cell viability. NO and LDH level were measured by spectrophotometer method. The effect of catalpol against high glucose induced injury on ECV-304 was observed. The results showed that there were no obvious changes in cell viabilities of ECV-304 cultured in normal concentration of glucose medium among groups with different concentrations of catalpol. Compared with the control group, cell viability was significantly decreased (P<0.01), the NO secretion was significantly reduced (P< 0.01), the LDH level was increased obviously (P<0.01) in the high glucose (30 mmol·L-1 glucose) injury model group. The high osmotic (24.5 mmol·L-1 mannitol) group was set up as a positive control. Comparison between the low dose (1 ng·μL-1 catalpol + 30 mmol·L-1 glucose), middle dose (10 ng·μL-1 catalpol + 30 mmol·L-1 glucose), and high glucose (30 mmol·L-1 glucose) injury model group showed no changes on cell viability and NO (P>0.05); while the LDH level was reduced (P<0.01). Comparison between the high dose catalpol (100 ng·μL-1 catalpol + 30 mmol·L-1 glucose) group and the high glucose model group showed that the cell viability was obviously increased (P<0.01); NO secretion was increased (P<0.05); and the LDH level was obviously reduced (P<0.01). It was concluded that catalpol had protective effect against high glucose induced ECV-304 injury through the regulation of NO and LDH level. The effect of high dose was obvious.

国家自然科学基金委面上项目（81273838）：针刺减肥的STAT5-miR-193 b信号通路中枢调控及机制研究，负责人：朱冰梅；教育部高等学校博士点基金博导类（20123237110001）：针刺减肥的STAT5-miR-193 b信号通路中枢调控及机制研究，负责人：朱冰梅；教育部新教师类（20133237120002）：组蛋白去乙酰化酶（HDACs）介导的电针抗缺血性脑中风研究，负责人：傅淑平；江苏省教育厅重大项目（11KJA360003）：转录因子STAT5在针刺减肥的中枢机制研究，负责人：朱冰梅。