一氧化氮与光化学法诱导大鼠脑缺血早期损伤的关系和绞股蓝总皂苷对脑缺血损伤的保护作用

目的：探讨一氧化氮(NO)与光化学法诱导大鼠脑缺血早期损伤的关系和绞股蓝总皂苷(Gyp)对脑缺血损伤的保护作用。方法：应用光化学法诱导大鼠大脑中动脉栓塞(MCAO)模型，观察氧合血红蛋白(OHb)和Gyp对MCAO后脑梗死范围，脑组织含水量、NO及超氧化歧化酶(SOD)、脂质过氧化产物TBARS含量的影响。结果：MCAO6h可导致大鼠局部脑组织明显梗死、脑水肿，同时SOD活力下降，TBARS含量升高，NO释放减少。OHb能进一步强化上述改变而Gyp能逆转上述变化。结论：脑内过氧化反应水平增高导致早期NO含量减少是脑缺血形成的重要原因之一，Gyp可通过影响脑缺血损伤早期脑内NO水平发挥对脑缺血的保护作用。

Relationship between nitric oxide and early ischemic brain damage induced by photochemistry in rats and the protective effects of gypenosides on the damage

AIM: To investigate the relatio ns hip between nitric oxide (NO) and early ischemic brain damage induced by photoch emistry and the effect of gypenosides (Gyp) on the damage. METHODS: The effects of Gyp and oxidized hemoglobin (OHb) on ischemic brain tissure areas, TBARS and H 2O contents, superoxide dismutase (SOD) activity and NO leve l were observed on the rat middle cerebral artery occlusion (MCAO) model induced by photochemistry. RESULTS: The middle cerebral artery occlusio n for 6 h caused obvious ischemic brain damage, increased the areas of ischemic brain and the contents of H 2O and TBARS, and decreased SOD activity and NO lev el (all P< 0.05 ). These effects can be exacerbated seriously by OHb, but reversed by Gyp. CONCLUSION: The decrease of early c erebral NO level is an important factor to lead to ischemic brain damage. Gyp de creases ischemic brain damage by increasing early cerebral NO level and has a pr ophylactic protective effect on cerebral ischemic damage.