The use of anesthetics relieves discomfort in patients during operation, but extensive application of anesthetics can cause damage to the nervous system. Atractylenolide III (ATL-III) is an active ingredient derived from Baizhu, which is a kind of traditional Chinese medicines. Recent studies have shown that ATL-III alleviates inflammation and oxidative stress in various tissues by regulating the PI3K/Akt/mTOR signaling pathway. However, whether or not the application of ATL-III could relieve isoflurane-induced damage in rat hippocampal neurons remains unclear. In this study, rats were stimulated with isoflurane and treated with ATL-III (intragastric administration) simultaneously. After rats were sacrificed, apoptosis and autophagy in the hippocampal neurons were assessed using TUNEL assays and western blotting, respectively. Then, the expression of inflammatory factors was determined by q-PCR and ELISA. The levels of p-PI3K, p-Akt, and p-mTOR were quantified by western blotting. We found that ATL-III relieved isoflurane-induced apoptosis, autophagy and inflammation in hippocampal neurons in rats. ATL-III treatment also inhibited the expression of TNF-α, IL-1β, and IL-6 in these cells. Furthermore, ATL-III promoted the expression of p-PI3K, p-Akt, and p-mTOR in the hippocampal neurons. All these results indicated that ATL-III alleviated isoflurane-induced injury in rat hippocampal neurons by activating the PI3K/Akt/mTOR signaling pathway.

中文翻译：

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苍术内酯 III 通过激活 PI3K/Akt/mTOR 通路减轻异氟醚诱导的大鼠海马神经元损伤

麻醉剂的使用可以缓解患者在手术过程中的不适感，但大量使用麻醉剂会对神经系统造成损害。白术内酯III（ATL-III）是一种来源于中药白术的有效成分。最近的研究表明，ATL-III 通过调节 PI3K/Akt/mTOR 信号通路减轻各种组织的炎症和氧化应激。然而，ATL-III的应用是否可以缓解异氟醚引起的大鼠海马神经元损伤尚不清楚。在这项研究中，大鼠用异氟醚刺激并同时用 ATL-III（胃内给药）治疗。处死大鼠后，分别使用 TUNEL 测定和蛋白质印迹法评估海马神经元的凋亡和自噬。然后，q-PCR和ELISA检测炎症因子的表达。p-PI3K、p-Akt 和 p-mTOR 的水平通过蛋白质印迹法定量。我们发现 ATL-III 减轻了异氟醚诱导的大鼠海马神经元凋亡、自噬和炎症。ATL-III 处理还抑制了这些细胞中 TNF-α、IL-1β 和 IL-6 的表达。此外，ATL-III 促进了海马神经元中 p-PI3K、p-Akt 和 p-mTOR 的表达。所有这些结果表明，ATL-III 通过激活 PI3K/Akt/mTOR 信号通路减轻异氟醚诱导的大鼠海马神经元损伤。大鼠海马神经元的自噬和炎症。ATL-III 处理还抑制了这些细胞中 TNF-α、IL-1β 和 IL-6 的表达。此外，ATL-III 促进了海马神经元中 p-PI3K、p-Akt 和 p-mTOR 的表达。所有这些结果表明，ATL-III 通过激活 PI3K/Akt/mTOR 信号通路减轻异氟醚诱导的大鼠海马神经元损伤。大鼠海马神经元的自噬和炎症。ATL-III 处理还抑制了这些细胞中 TNF-α、IL-1β 和 IL-6 的表达。此外，ATL-III 促进了海马神经元中 p-PI3K、p-Akt 和 p-mTOR 的表达。所有这些结果表明，ATL-III 通过激活 PI3K/Akt/mTOR 信号通路减轻异氟醚诱导的大鼠海马神经元损伤。