Lyu Zhipai, Cao Jing, Wang Ju, Lian Hongmei
Department of Anesthesia, The Third Affiliated Hospital of Zhengzhou University, Henan, Zhengzhou 450052, P.R. China.
Department of Pathology, The Third Affiliated Hospital of Zhengzhou University, Henan, Zhengzhou 450052, P.R. China.
Exp Ther Med. 2018 Mar;15(3):3117-3123. doi: 10.3892/etm.2018.5758. Epub 2018 Jan 17.
Previous studies have demonstrated that Vitexin possesses antihypertensive, anti-inflammatory and potential anticancer effects. The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase-3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane-induced newborn rats. In addition, Vitexin pretreatment increased superoxide dismutase and glutathione peroxidase activity. Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF-1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated-p38 MAP kinase (p38) protein expression in sevoflurane-induced newborn rat. Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α-, VEGF- and p38-associated signaling pathways in newborn rats.
先前的研究表明，牡荆素具有抗高血压、抗炎和潜在的抗癌作用。本研究旨在探讨牡荆素的保护作用是否能抵御七氟醚诱导的神经元凋亡以及这种保护作用的潜在机制。结果表明，在七氟醚诱导的新生大鼠中，牡荆素预处理显著减少了神经元凋亡，并抑制了半胱天冬酶-3活性、凋亡调节因子BAX蛋白表达和丙二醛水平。此外，牡荆素预处理增加了超氧化物歧化酶和谷胱甘肽过氧化物酶活性。此外，研究发现，在七氟醚诱导的新生大鼠中，牡荆素处理可诱导缺氧诱导因子1α亚基（HIF-1α）和血管内皮生长因子（VEGF）蛋白表达，并抑制磷酸化p38丝裂原活化蛋白激酶（p38）蛋白表达。总之，本研究结果表明，牡荆素的保护作用通过新生大鼠中与HIF-1α、VEGF和p38相关的信号通路减少了七氟醚诱导的神经元凋亡。
