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人参皂甙-Rd对氯胺酮诱导幼年大鼠海马神经元凋亡的影响
Influence of ginsenoside-Rd injection on ketamine-induced neuroapoptosis in the infant rat hippocampus
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DOI:
作者:
杨周晶
YANG Zhoujing
作者单位:
上海交通大学附属新华医院麻醉与重症医学科
Department of Anesthesiology and Critical Care, Xinhua Hospital
关键词:
氯胺酮;GSRd;幼鼠;海马;凋亡
ketamine; GSRd; Neonatal rats; hippocampus; apoptosis
摘要:
【摘要】 目的 探讨人参皂甙Rd注射液(ginsenoside-Rd,GSRd)对于氯胺酮诱导幼年大鼠海马神经元凋亡的影响。方法 幼年SD雄性大鼠,随机分为对照组(C组)、氯胺酮麻醉组(K组)、氯胺酮+ GSRd预处理高剂量组(K+HG)、氯胺酮+ GSRd预处理低剂量组(K+LG)、人参皂甙组(G组)。K组、K+HG、K+LG组的大鼠在出生后第7天(P7)均予以腹腔注射氯胺酮80 mg/kg。其中K+HG组于氯胺酮注射前48 h,24 h和0.2 h时,连续3次腹腔注射GSRd 100 mg/kg,K+LG组于氯胺酮注射前48 h,24 h和0.2 h时,连续3次腹腔注射GSRd 5~40 mg/kg。C组的大鼠在出生后第7天(P7)予以腹腔注射等剂量生理盐水代替氯胺酮。G组于氯胺酮麻醉时间点前48 h,24 h 0.2 h时,连续3次腹腔注射GSRd 100 mg/kg,但不给予氯胺酮麻醉处理。待K组、K+HG组、K+LG组的大鼠苏醒后即刻处死,用westernblot的方法检测不同处理组中P7大鼠的海马神经元活性caspase 3与Bax的表达水平,记录不同剂量的GSRd对氯胺酮诱导P7大鼠海马神经元凋亡的影响。结果 经氯胺酮麻醉处理后,P7大鼠的海马神经元活性caspase 3、Bax的表达明显升高(P<0.05),加入GSRd 5~40 mg/kg剂量的预处理不影响氯胺酮诱导的P7大鼠的海马神经元活性caspase 3、Bax的表达,GSRd 100 mg/kg剂量的预处理可进一步增加氯胺酮诱导的P7大鼠海马神经元活性caspase 3、Bax的表达(P<0.05)。结论 低剂量GSRd 对氯胺酮诱导的幼年大鼠的海马神经元凋亡没有影响,而高剂量 GSRd 增加了海马神经元的凋亡。GSRd 对于氯胺酮诱导的幼年大鼠的海马神经元凋亡没有保护作用。
【Abstract】 Objective To identify the influence of ginsenoside-Rd (GSRd) injection on ketamine induced neuroapoptosis in the infant rat hippocampus. Methods The Sprague-Dawley rat pups were randomly divided into five groups (n=5):(1) Control group (group C) (2) ketamine group (group K) (3) ketamine +pretreatment with high dose of GSRd (group K+HG) (4) ketamine + pretreatment with low dose of GSRd (group K+LG) (5) GSRd group (group G). Group K, Group K+HG and Group K+LG were injected intraperitoneally with 80 mg/kg ketamine seven days after birth. Apart from these, Group K+HG was intraperitoneally with 100 mg/kg GSRd consecutively at 48 h, 24 h and 0.2 h before ketamine exposure. Group K+LG was intraperitoneally with 5-40 mg/kg GSRd consecutively at 48 h, 24 h and 0.2 h before ketamine exposure. Group C was injected intraperitoneally with same volume of saline in place of ketamine treatment. Group G was intraperitoneally with 100mg/kg GSRd consecutively at 48 h, 24 h and 0.2 h before the time point of ketamine exposure but it did not receive ketamine treatment. When Group K, Group K+HG, Group K+LG rats revived,they were killed.Western blot was used to analyze the expression of activated caspase 3, Bax of five different groups in the hippocampus of the rat pups. Results We found that activated caspase 3 and Bax expression were upregulated in the hippocampus of P7 rat pups following ketamine treatment (P<0.05). Preconditioning with GSRd (5-40 mg/kg) could not attenuate the increase of activated caspase 3 and Bax induced by ketamine. Preconditioning with GSRd (100 mg/kg) increased the expression of activated caspase 3 and Bax induced by ketamine (P<0.05). Conclusion Our study indicated that low dose of GSRd did not reserve increase of ketamine-induced neuronal apoptosis in hippocampus while high dose of GSRd promoted neurodegeneration. GSRd did not serve anti-apoptotic function against ketamine-induced cell loss in the rat pups hippocampus.
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