摘要
用ＮＡＤＰＨｄ 组织化学和电镜技术研究了汉防己碱（Ｔｅｔ）对大鼠缺血再灌流脑一氧化氮合酶（ＮＯＳ）活性及超微结构变化的作用。结果发现，缺血１５ ｍ ｉｎ，再灌流２ ｈ 后，海马超微结构出现明显的病理学损害，主要包括核周出现髓鞘样变，核周间隙增大，胞核均质化，大量片状软化灶，毛细血管周围水肿。Ｔｅｔ １０ 和２０ｍ ｇ／ｋｇ 缺血前３０ ｍ ｉｎ 腹腔注射可明显改善或避免出现上述缺血组织学改变。缺血１５ ｍ ｉｎ，再灌流２４ ｈ 后，皮层和海马ＮＯＳ阳性细胞数目显著增多，Ｔｅｔ５，１０ 和１５ ｍ ｇ／ｋｇ 缺血前３０ ｍ ｉｎ 腹腔注射，浓度依赖地抑制缺血再灌流所致的ＮＯＳ阳性细胞数目增加。这些结果提示，Ｔｅｔ可抑制缺血再灌流脑ＮＯＳ活性，减少ＮＯ产生，这可能与Ｔｅｔ减轻脑缺血再灌流的损害有关。
Effects of tetrandrine (Tet) on the changes of NOS activity and ultrastructure were studied in rat ischemia and reperfusion brain by using NADPH diaphorase histochemistry and electroscope technique. After 15 min ischemia and 2 h reperfusion, ultrastructures of hippocampus showed pathological morphological changes. The most striking alterations consisted of myelinfigure and edema around the nucleus, and capillaries, homogenization of nucleus, large numbers of softening focuses. Tet (10 and 20 mg/kg, ip) 30 min before ischemia reduced or even averted the pathological changes. 24 h after ischemia reperfusion, the number of NOS positive cells in cortex and hippocampus increased significantly as compared with the control. Tet (5,10, and 15 mg/kg ip) 30 min before ischemia inhibited the increase in dose dependent manner. The results suggest that Tet may protect the cerebral ischemic injury probably by inhibiting the overloaded production of NO.
关键词
脑缺血
再灌注损伤
NOS
超微结构
汉防己碱
ischemia/reperfusion
hippocampus
cortex
NOS
ultrastructure
tetrandrine
