实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
20期
3219-3222
,共4页
氧糖剥夺%miR-184%AKT2%缺血损伤
氧糖剝奪%miR-184%AKT2%缺血損傷
양당박탈%miR-184%AKT2%결혈손상
Oxygen-glucose-deprivation%miR-184%AKT2%Ischemic injury
目的:探讨miR-184在氧糖剥夺(OGD)诱导SK-N-SH细胞缺血缺氧损伤中的作用及其对抗凋亡基因AKT2的调节。方法:应用RT-PCR检测miR-184在SK-N-SH细胞OGD后的表达情况,并瞬时转染miR-184的类似物、抑制物及其阴性对照,分别行RT-PCR检测miR-184和AKT2的表达,MTT染色检测细胞存活率。结果:与正常细胞相比,miR-184在OGD诱导的缺血损伤模型中表达下调(P<0.05);且过表达或抑制miR-184可显著改变AKT2的表达,影响缺血损伤细胞的存活率(P<0.05);而在非OGD作用下,miR-184对SK-N-SH细胞的活力无显著影响。结论:miR-184通过负性调节AKT2的表达水平,在OGD诱导的缺血损伤中发挥重要作用。
目的:探討miR-184在氧糖剝奪(OGD)誘導SK-N-SH細胞缺血缺氧損傷中的作用及其對抗凋亡基因AKT2的調節。方法:應用RT-PCR檢測miR-184在SK-N-SH細胞OGD後的錶達情況,併瞬時轉染miR-184的類似物、抑製物及其陰性對照,分彆行RT-PCR檢測miR-184和AKT2的錶達,MTT染色檢測細胞存活率。結果:與正常細胞相比,miR-184在OGD誘導的缺血損傷模型中錶達下調(P<0.05);且過錶達或抑製miR-184可顯著改變AKT2的錶達,影響缺血損傷細胞的存活率(P<0.05);而在非OGD作用下,miR-184對SK-N-SH細胞的活力無顯著影響。結論:miR-184通過負性調節AKT2的錶達水平,在OGD誘導的缺血損傷中髮揮重要作用。
목적:탐토miR-184재양당박탈(OGD)유도SK-N-SH세포결혈결양손상중적작용급기대항조망기인AKT2적조절。방법:응용RT-PCR검측miR-184재SK-N-SH세포OGD후적표체정황,병순시전염miR-184적유사물、억제물급기음성대조,분별행RT-PCR검측miR-184화AKT2적표체,MTT염색검측세포존활솔。결과:여정상세포상비,miR-184재OGD유도적결혈손상모형중표체하조(P<0.05);차과표체혹억제miR-184가현저개변AKT2적표체,영향결혈손상세포적존활솔(P<0.05);이재비OGD작용하,miR-184대SK-N-SH세포적활력무현저영향。결론:miR-184통과부성조절AKT2적표체수평,재OGD유도적결혈손상중발휘중요작용。
Objective To explore the role of miR-184 in Oxygen-Glucose-Deprivation (OGD) induced SK-N-SH cell ischemic injury and its regulation on AKT2 level. Method We used a combination of oxygen and glucose deprivation to imitate ischemic conditions in vivo. MiR-184 mimic and inhibitor were transfected into SK-N-SH cell to alter miR-184 levels. The expression of miR-184 and AKT2 were determined by using Real-time PCR. The extent of SK-N-SH cell survival rate was assessed by thiazolyl blue tetrazolium bromide (MTT) assay. Result Here, we observed that miR-184 was significantly inhibited in SK-N-SH cell after OGD (P<0.05). The changes of miR-184 level altered the expression of AKT2 mRNA. In addition, alteration of miR-184expressionsignificantly affected cell survival rate after OGD. Conclusion miR-184 plays an important role in ischemic injury through negatively regulating AKT2 level, which may provide a potential therapeutic target for ischemic stroke in miRNA levels.