摘要
目的研究δ阿片受体激动剂DPDPE对原代培养的大鼠皮层神经元缺氧无糖损伤(OGD)的保护作用并探讨其机制。方法将大鼠皮层神经元分为4组,共24孔、每组6孔:正常氧浓度组;缺氧组;缺氧+DP-DPE(终浓度为100nmol/L)预处理组;缺氧+DPDPE+Naltrindole(δ阿片受体拮抗剂,终浓度为1μmol/L)预处理组。通过采用LDH观察DPDPE对于神经元缺氧无糖损伤的保护作用;用Western检测大鼠皮层神经元中pERK、pp38、Bcl-2和Bax等蛋白表达的变化。结果 (1)与正常对照组相比,缺氧无糖损伤4h细胞上清液中LDH水平明显升高(P<0.01),加不同浓度DPDPE预处理后LDH水平明显降低(P<0.01);与缺氧无糖组相比,DPDPE预处理显著增加pERK的蛋白表达(P<0.05)且同时降低pp38的蛋白表达(P<0.05),该作用可部分的被Nal-trindole所阻断;与缺氧无糖组相比,DPDPE预处理显著增加抗凋亡蛋白Bcl-2的表达(P<0.05)且同时降低凋亡蛋白Bax的表达(P<0.05)。结论 DPDPE对于大鼠原代皮层神经元缺氧无糖(OGD)损伤具有明显的保护效果,其作用机制与增加pERK,降低pp38的蛋白表达,以及调节Bcl-2/Bax的表达有关。
Objective To detect if DPDPE can protect the cultured rat cortical neurons from oxygen - glucose deprivation （OGD） injury and elucidate the underlying mechanism. Methods Cortical neurons were divided into 4 groups ： Control （ n = 6）, OGD （ n = 6 ）, DPDPE ＋ OGD （ n = 6 ）, DPDPE ＋ Naltrindole （NTI） ＋ OGD （ n = 6 ）. Neuron injury were assessed by lactate dehydrogenase （LDH） release. Protein expression was examined by Western blot analysis. Results It is increased dramatically of LDH level in ODG group compared with Control group and it can be decreased by DPDPE pretreatment. DPDPE induced a major increase in pERK（ P 〈 0. 05 ）and Bcl -2 levels （P 〈 0. 05 ）. It also prevented the increase in pp38 （ P 〈 0. 05 ） and Bax （ P 〈 0. 05 ） in neurons during OGD. Neither DPDPE nor nahrindole had any appreciable effect on the levels of pJNK. Conclusion DPDPE protect the cortical neuron dose - dependly from OGD injury. One of the protective mechanism of DPDPE may be due to the dynamic balance between the pERK and the pp38.
出处
《广东医学》
CAS
CSCD
北大核心
2012年第15期2206-2209,共4页
Guangdong Medical Journal
基金
贝朗麻醉科学研究基金资助项目(编号:H012011020)
