CAJ | 학술논문

本文旨在探讨莪术油注射液对慢性低氧大鼠学习与记忆的影响及其可能机制.将Sprague.Dawley大鼠随机分为对照组、慢性低氧组、5 mg/kg体重莪术油组、10 mg/kg体重莪术油组、20 mg/kg体重莪术油组,每组14只.慢性低氧处理采用低氧舱内吸入大约10%O2、5%CO2,饲养10 h/d,持续饲养28 d.莪术油组大鼠低氧处理前腹腔注射相应浓度的莪术油注射液.实验结束次日,通过Morris水迷宫测试各组动物学习和记忆成绩的变化;测定各组大鼠血清和海马组织丙二醛(malonaldehyde,MDA)含量和超氧化物歧化酶(superoxide dismutase,SOD)活性以及海马组织Ca2+浓度([Ca2+i]);通过免疫组织化学和Western blot检测磷酸化Ca2+/钙调蛋白依赖性蛋白激酶Ⅱ(phosphorylated Ca2+/calmodulin-dependent pro-tein kinase Ⅱ,p-CaMKII)在海马组织和胞膜上的表达.结果显示,与对照组相比,慢性低氧组大鼠隐蔽平台的逃避潜伏期明显延长(P<0.05),血清和海马组织MDA含量明显增高,SOD活性显著降低(P<0.05,P<0.01),海马组织[Ca2+]i明显增高(P<0.01),海马P-CaMKII表达量显著降低(P<0.01).与慢性低氧组比较,莪术油各组发生以下变化:10、20 mg/kg体重莪术油组大鼠隐蔽平台的逃避潜伏期显著缩短(P<0.05):5、10、20 mg/kg体重莪术油组大鼠血清和海马组织MDA含量均显著降低(P<O.05,P<0.01);10、20 mg/kg体重莪术油组大鼠血清SOD活性显著增加(P<0.01);5、10、20 mg/kg体重莪术油组大鼠海马组织[Ca2+]i明显降低(P<0.01);10、20 mg/kg体重莪术油组大鼠海马p-CaMKII表达也明显增加(P<O.05,P<0.01).以上结果提示,莪术油改善慢性低氧导致的大鼠学习与记忆能力下降,其机制可能与降低血清和海马组织MDA含量、增加SOD活性、降低海马组织[Ca2+];和/或增加海马组织p-CaMKII表达有关.
본문지재탐토아술유주사액대만성저양대서학습여기억적영향급기가능궤제.장Sprague.Dawley대서수궤분위대조조、만성저양조、5 mg/kg체중아술유조、10 mg/kg체중아술유조、20 mg/kg체중아술유조,매조14지.만성저양처리채용저양창내흡입대약10%O2、5%CO2,사양10 h/d,지속사양28 d.아술유조대서저양처리전복강주사상응농도적아술유주사액.실험결속차일,통과Morris수미궁측시각조동물학습화기억성적적변화;측정각조대서혈청화해마조직병이철(malonaldehyde,MDA)함량화초양화물기화매(superoxide dismutase,SOD)활성이급해마조직Ca2+농도([Ca2+i]);통과면역조직화학화Western blot검측린산화Ca2+/개조단백의뢰성단백격매Ⅱ(phosphorylated Ca2+/calmodulin-dependent pro-tein kinase Ⅱ,p-CaMKII)재해마조직화포막상적표체.결과현시,여대조조상비,만성저양조대서은폐평태적도피잠복기명현연장(P<0.05),혈청화해마조직MDA함량명현증고,SOD활성현저강저(P<0.05,P<0.01),해마조직[Ca2+]i명현증고(P<0.01),해마P-CaMKII표체량현저강저(P<0.01).여만성저양조비교,아술유각조발생이하변화:10、20 mg/kg체중아술유조대서은폐평태적도피잠복기현저축단(P<0.05):5、10、20 mg/kg체중아술유조대서혈청화해마조직MDA함량균현저강저(P<O.05,P<0.01);10、20 mg/kg체중아술유조대서혈청SOD활성현저증가(P<0.01);5、10、20 mg/kg체중아술유조대서해마조직[Ca2+]i명현강저(P<0.01);10、20 mg/kg체중아술유조대서해마p-CaMKII표체야명현증가(P<O.05,P<0.01).이상결과제시,아술유개선만성저양도치적대서학습여기억능력하강,기궤제가능여강저혈청화해마조직MDA함량、증가SOD활성、강저해마조직[Ca2+];화/혹증가해마조직p-CaMKII표체유관.
The effect of Rhizoma curcumae oil on the learning and memory in rats exposed to chronic hypoxia and the possible mechanismswere investigated. The rats were divided randomly into 5 groups (14 animals in each group): control, chronic hypoxia, chronic hypoxiawith low (5 mg/kg body weight), middle (10 mg/kg body weight) and high (20 mg/kg body weight) concentrations of Rhizoma curcumaeoil injection. The animals undergoing chronic hypoxia were exposed to hypoxia in a hypoxic chamber containing 10% O2 and 5% CO2 for 10 h/d, lasting 28 d. Morris water maze (MWM) test was used to obtain the scores of leaning and memory. The superoxide dismutase(SOD) activity and malonaldehyde (MDA) content were determined in the serum and hippocampus as well as [Ca2+]I in the hippocampus.The expression of phosphorylated Ca2+/calmodulin-dependent protein kinase Ⅱ (p-CaMKII) in the hippocampus was evaluated by usingimmunohistochemistry and Western blot. Compared with the control group, the chronic hypoxia group showed the following changes:(1) The escape latency to the hidden platform was remarkably prolonged (P<0.05); (2) The content of MDA and [Ca2+]I were obviouslyhigher, but the activity of SOD and the expression of p-CaMKII were significantly lower (P<0.05, P<0.01). Compared with the chronic hypoxia group, groups with Rhizoma curcumae oil injection had the following changes: (1) The escape latency to the hidden platform was remarkably shorter in 10, 20 mg/kg body weight groups (P<0.05); (2) The content of MDA and [Ca2+]I were markedly decreased in 5, 10, 20 mg/kg body weight groups (P<0.05, P<0.01), but the activity of SOD in the serum and the expression of p-CaMKII were significantly higher in 10, 20 mg/kg body weight groups (P<0.05, P<0.01). The results showed that the capacity of learning and memory was degraded following chronic hypoxia. The decrease in MDA content and [Ca2+]I and (or) the increase in SOD activity and p-CaMKII expression might participate in the enhancing effect on learning and memory induced by Rhizoma curcumae oil.