Trigonelline is a plant alkaloid that has generated interest for its neuroprotective roles in brain pathology. However, the protective effect of trigonelline on cerebral ischemia/reperfusion (I/R) injury and the potential mechanism have not been fully evaluated. Our results showed that trigonelline pretreatment ameliorated oxygen-glucose deprivation/reperfusion (OGD/R)-induced hippocampal neurons injury. The OGD/R-caused reactive oxygen species (ROS) generation and decreased concentrations of superoxide dismutases (SOD) and glutathione peroxidase (GPx) were markedly attenuated by trigonelline. In addition, the increased levels of TNF-α, IL-6 and IL-1β in OGD/R-induced hippocampal neurons were significantly decreased by trigonelline pretreatment. Trigonelline also suppressed caspase-3 activity and bax expression, and induced bcl-2 expression in OGD/R-induced hippocampal neurons. Furthermore, trigonelline induced the activation of PI3K/Akt pathway in hippocampal neurons exposed to OGD/R condition. Inhibition of PI3K/Akt signaling reversed the protective effects of trigonelline on OGD/R-induced hippocampal neurons injury. Taken together, these findings indicated that trigonelline protected hippocampal neurons from OGD/R-induced injury, which was mediated by the activation of PI3K/Akt signaling pathway.

中文翻译：

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Trigonelline通过激活PI3K / Akt途径保护海马神经元免受氧葡萄糖剥夺引起的损伤。

Trigonelline是一种植物生物碱，因其在脑病理学中的神经保护作用而引起人们的兴趣。然而，曲安奈林对脑缺血/再灌注（I / R）损伤的保护作用及其潜在机制尚未得到充分评估。我们的研究结果表明，曲安奈林预处理可改善氧葡萄糖剥夺/再灌注（OGD / R）诱导的海马神经元损伤。三角果碱显着减弱了OGD / R引起的活性氧（ROS）的产生以及超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）浓度的降低。此外，曲安奈林预处理可显着降低OGD / R诱导的海马神经元中TNF-α，IL-6和IL-1β的水平升高。Trigonelline还抑制caspase-3活性和bax表达，和在OGD / R诱导的海马神经元中诱导bcl-2表达。此外，曲古吉林诱导了暴露于OGD / R条件的海马神经元中PI3K / Akt途径的激活。PI3K / Akt信号的抑制逆转了trigonelline对OGD / R诱导的海马神经元损伤的保护作用。综上所述，这些发现表明曲古萘林保护海马神经元免受OGD / R诱导的损伤，这是由PI3K / Akt信号通路的激活介导的。