活力测定
MTT法
氧化应激
蛋白激酶B
PI3K/AKT/mTOR通路
活性氧
细胞凋亡
超氧化物歧化酶
化学
丙二醛
二氯荧光素
药理学
神经保护
谷胱甘肽过氧化物酶
再灌注损伤
分子生物学
生物
生物化学
缺血
医学
内科学
作者
Yuxin Liu,Xianchuang Wu,Jing An,Weiling Lv,Yan-Na Geng,Tingting Lou,Yongzhou Zhang
摘要
Abstract Oxidative stress has been implicated in the development of cerebral ischemia/reperfusion (I/R) injury. Glaucocalyxin B (GLB), one of five ent‐kauranoid diterpenoids, was reported to possess neuroprotective activity. However, the effect of GLB on oxygen‐glucose‐deprivation/reperfusion (OGD/R)‐induced cell injury in PC‐12 cells has not been explored. PC‐12 cells was treated with various concentrations of GLB (0, 2.5, 5 and 10 μM), and cell viability was detected using the MTT assay. PC‐12 cells were pretreated with the indicated concentration of GLB (2.5‐10 μM, 2 hours pretreatment), and were maintained under OGD for 3 hours, followed by 24 hours of reoxygenation. Cell viability was assessed using the MTT assay. The levels of superoxide dismutase, malondialdehyde, and glutathione peroxidase were detected using commercially available ELISA Kits. Intracellular reactive oxygen species level was measured using the fluorescent probe 2′,7′‐dichlorofluorescein diacetate. The levels of Bcl‐2, Bax, p‐Akt, Akt, p‐mTOR, mTOR were detected using Western blot. Our results revealed that GLB significantly protected PC12 cells against OGD/R‐induced cell injury. In addition, GLB efficiently inhibited oxidative stress and cell apoptosis in OGD/R‐stimulated PC‐12 cells. Mechanistic studies revealed that pretreatment with GLB could induce the activation of Akt/mTOR signaling pathway resulting in protection of OGD‐treated PC12 cells. In conclusion, our data indicate for the first time that GLB protects against OGD/R‐induced neuronal injury in PC‐12 cells. The mechanism of the protective effect of GLB is partially associated with activation of the Akt/mTOR signaling pathway. Thus, GLB may be a potential agent for protection against cerebral I/R injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI