Pachymic acid (PA) from medicinal fungus Poria cocos has a variety of pharmacological potentials. However, there are no reports of the effects of PA on cerebral ischemia/reperfusion (I/R) injury. The purpose of this study was to investigate the mechanisms of PA on cerebral I/R injury in rats. The effects of PA on cerebral infarction size, brain water content, neurological symptoms and cerebral blood flow were evaluated. Nissl staining was used to observe the damage of ischemic brain neurons after I/R in rats. Apoptosis of ischemic brain neurons after I/R was observed by TUNEL staining. The effect of PA on the expression of some components of PI3K/Akt was detected by Western blotting. PA significantly increased cerebral blood flow after I/R in rats, reduced infarct volume and brain water content, and downgrade neurological function scores, significantly reduced neuronal damage after I/R in rats, and significantly decreased neuronal apoptosis. The effect of PA on rat I/R can be eliminated by LY294002. In addition, PA significantly up-regulated the protein expression of p-PTEN (Ser380), p-PDK1 (Ser241), p-Akt (Ser473), pc-Raf (Ser259) and p-BAD (Ser136), and down-regulated Cleaved caspase protein expression. LY294002 can reverse the effect of PA on the expression of PI3K / Akt signaling pathway related protein in rats after I/R. PA had obviously neuroprotective effects on brain I/R injury and neuronal apoptosis, and its mechanism may be related to activation of PI3K / Akt signaling pathway.

中文翻译：

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厚朴酸通过PI3K / Akt信号传导通路保护脑缺血/再灌注损伤。

药用真菌Por（Poria cocos）中的酸（PA）具有多种药理潜力。但是，没有关于PA对脑缺血/再灌注（I / R）损伤的影响的报道。这项研究的目的是调查PA对大鼠脑I / R损伤的机制。评估了PA对脑梗死面积，脑含水量，神经系统症状和脑血流量的影响。Nissl染色用于观察大鼠缺血再灌注后缺血性脑神经元的损伤。通过TUNEL染色观察到I / R后缺血性脑神经元的凋亡。通过Western印迹检测PA对PI3K / Akt某些成分表达的影响。PA显着增加了大鼠I / R后的脑血流量，减少了梗塞体积和脑含水量，并降低了神经功能评分，显着降低大鼠I / R后的神经元损伤，并显着降低神经元凋亡。LY294002可以消除PA对大鼠I / R的影响。此外，PA显着上调了p-PTEN（Ser380），p-PDK1（Ser241），p-Akt（Ser473），pc-Raf（Ser259）和p-BAD（Ser136）的蛋白表达，调节C裂半胱天冬酶蛋白的表达。LY294002可以逆转PA对I / R后大鼠PI3K / Akt信号通路相关蛋白表达的影响。PA对脑I / R损伤和神经元凋亡具有明显的神经保护作用，其机制可能与PI3K / Akt信号通路的激活有关。PA显着上调p-PTEN（Ser380），p-PDK1（Ser241），p-Akt（Ser473），pc-Raf（Ser259）和p-BAD（Ser136）的蛋白表达，并下调Cleaved caspase蛋白表达。LY294002可以逆转PA对I / R后大鼠PI3K / Akt信号通路相关蛋白表达的影响。PA对脑I / R损伤和神经元凋亡具有明显的神经保护作用，其机制可能与PI3K / Akt信号通路的激活有关。PA显着上调p-PTEN（Ser380），p-PDK1（Ser241），p-Akt（Ser473），pc-Raf（Ser259）和p-BAD（Ser136）的蛋白表达，并下调Cleaved caspase蛋白表达。LY294002可以逆转PA对I / R后大鼠PI3K / Akt信号通路相关蛋白表达的影响。PA对脑I / R损伤和神经元凋亡具有明显的神经保护作用，其机制可能与PI3K / Akt信号通路的激活有关。