CAJ | 학술논문

从细胞和分子水平探讨半胱胺(cysteamine,CS)对1-甲基-4-苯基吡啶离子(MPP+)诱导的 SH-SY5Y细胞毒性模型的保护作用及作用机制。方法以 MPP+做为毒物建立 SH-SY5Y细胞损伤模型；通过四甲基偶氮唑盐(MTT)定量观察CS对 MPP+诱导的 SH-SY5Y细胞模型的保护作用；检测氧化应激指标：丙二醛(MDA),细胞内活性氧(ROS)；抗氧化物谷胱甘肽(GSH),探讨 CS 的保护机制。结果①CS 预处理细胞24小时后再给以MPP+处理 SY5Y细胞,CS 400μmol/L细胞存活率最高。②CS 400μmol/L预处理细胞能够有效的降低 MPP+诱导的细胞内 ROS、MDA氧化应激指标。③CS 400μmol/L 预处理细胞能够显著地促进细胞内抗氧化剂 GSH 的增加。结论 CS可能是通过抑制氧化应激,促进细胞内 GSH 合成发挥神经保护作用。
종세포화분자수평탐토반광알(cysteamine,CS)대1-갑기-4-분기필정리자(MPP+)유도적 SH-SY5Y세포독성모형적보호작용급작용궤제。방법이 MPP+주위독물건립 SH-SY5Y세포손상모형；통과사갑기우담서염(MTT)정량관찰CS대 MPP+유도적 SH-SY5Y세포모형적보호작용；검측양화응격지표：병이철(MDA),세포내활성양(ROS)；항양화물곡광감태(GSH),탐토 CS 적보호궤제。결과①CS 예처리세포24소시후재급이MPP+처리 SY5Y세포,CS 400μmol/L세포존활솔최고。②CS 400μmol/L예처리세포능구유효적강저 MPP+유도적세포내 ROS、MDA양화응격지표。③CS 400μmol/L 예처리세포능구현저지촉진세포내항양화제 GSH 적증가。결론 CS가능시통과억제양화응격,촉진세포내 GSH 합성발휘신경보호작용。
To investigate the neuroprotective effect and underlying machanism of cysteamine on 1-methy1-4-phenylpyridinium(MPP+)induced SH-SY5Y cell model.Methods MPP+-induced SH-SY5Y cell model was established with the purpose of observation protective effect and the protection mechanism of cysteamine.The protection of cysteamine on MPP+ induced neurontoxicity was estimated by 3-[4,5-dimethylthiazol-2-yl ]-2,5-dipheryltetr azolium bromide(MTT).The underlying mechanism of neuroprotection was determined by oxidative stress indicators,such as:malondialdhyde(MDA),reaction oxygen(ROS),antioxidant antioxidant glutathione(GSH).Results①The highest cell survival rate was observed at the dose of cysteamine (CS)400μmol/L in MPP+ treated SY5Y cell model after CS pretreatment at 24 hours.② CS 400μmol/L pretreatment can effectively reduce the MPP+-induced intracellular ROS and MDA level.③CS 400 μmol/L pretreatment can significantly increase the cellular antioxidant GSH levels.Conclusion CS has neuroprotective effect in SY5Y cell models.The neuroprotective effect is likely through inhibiting the oxidative indicators,promoting synthesis of cellular GSH.