Wang Qi-Lin, Guo Chao, Qi Jie, Ma Jia-Hui, Liu Fang-Yuan, Lin Shi-Qi, Zhang Cai-Yun, Xie Wei-Dong, Zhuang Jing-Jing, Li Xia
a Marine College, Shandong University , Weihai 264209 , China.
b School of Pharmaceutical Science , Shandong University , Jinan 250012 , China.
J Asian Nat Prod Res. 2019 Apr;21(4):364-376. doi: 10.1080/10286020.2017.1423057. Epub 2018 Jan 21.
3β-Angeloyloxy-8β,10β-dihydroxyeremophila-7(11)-en-12,8α-lactone (FJ1) inhibited effectively paraquat (PQ)-induced injury in SH-SY5Y cells. In this way, FJ1 was shown to reverse the PQ-induced activation of caspase-9 and caspase-3, the increase in Bax/Bcl-2 ratio, and the release of cytochrome c. The mechanism was associated with a reduction of oxidative stress, including the decrease in the levels of ROS and MDA and maintaining the activity of SOD and GSH. Taken together, findings revealed that FJ1 had protective effects against PQ-induced injury via attenuating the oxidative stress in SH-SY5Y cells, which suggested that FJ1 might be a candidate for further evaluation against neurodegeneration in Parkinson's disease.
3β-当归酰氧基-8β,10β-二羟基澳洲茄-7(11)-烯-12,8α-内酯（FJ1）有效抑制了百草枯（PQ）诱导的SH-SY5Y细胞损伤。通过这种方式，FJ1被证明可逆转PQ诱导的半胱天冬酶-9和半胱天冬酶-3的激活、Bax/Bcl-2比值的增加以及细胞色素c的释放。其机制与氧化应激的降低有关，包括活性氧（ROS）和丙二醛（MDA）水平的降低以及超氧化物歧化酶（SOD）和谷胱甘肽（GSH）活性的维持。综上所述，研究结果表明FJ1通过减轻SH-SY5Y细胞中的氧化应激对PQ诱导的损伤具有保护作用，这表明FJ1可能是进一步评估用于对抗帕金森病神经退行性变的候选药物。
