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Neuroprotective effect of paeoniflorin on H2O2-induced apoptosis in PC12 cells by modulation of reactive oxygen species and the inflammatory response

机译:eon药苷通过调节活性氧和炎症反应对H2O2诱导PC12细胞凋亡的神经保护作用

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摘要

Paeoniflorin (PF) is a product derived from Paeoniae Radix and is commonly prescribed in traditional Chinese medicine. PF has been reported to exhibit neuroprotective, anti-ischemic, antioxidant, anti-inflammatory and anticancer effects. The neuroprotective properties of PF have been demonstrated in animal models of various neuropathologies. The present study investigated the effects of PF on hydrogen peroxide (H2O2)-induced apoptosis in PC12 cells, to improve the understanding of the mechanisms underlying its neuroprotective properties. The H2O2-induced apoptosis of PC12 cells resulted in a reduction in the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein ratio and the activation of caspase-3. PF treatment was observed to reverse the apoptotic process and to modulate the expression levels of a number of apoptosis-associated proteins. Furthermore, PF significantly mitigated the H2O2-induced reduction in cell viability, in addition to scavenging reactive oxygen species and preventing the release of lactate dehydrogenase from the PC12 cells. In addition, the apoptosis-associated activation of nuclear factor (NF)-κB was inhibited in the PF-treated cells, and the expression levels of tumor necrosis factor α and interleukin (IL)-1β were reduced. In conclusion, the present study demonstrated that PF was able to reduce H2O2-induced toxicity by blocking the activation of the neuroinflammatory factor NF-κB. These results suggest that PF may be a valuable neuroprotective agent for the treatment of neurological disease and injury.
机译:eon药苷(PF)是从Pa药中提取的产品,在传统中药中通常开处方。据报道,PF具有神经保护,抗缺血,抗氧化,抗炎和抗癌作用。 PF的神经保护特性已在各种神经病理学的动物模型中得到证实。本研究调查了PF对过氧化氢(H2O2)诱导的PC12细胞凋亡的影响,以增进对其神经保护特性潜在机制的了解。 H2O2诱导的PC12细胞凋亡导致B细胞淋巴瘤2(Bcl-2)/ Bcl-2相关的X蛋白比率降低和caspase-3激活。观察到PF处理可逆转凋亡过程并调节许多凋亡相关蛋白的表达水平。此外,除清除活性氧种类并防止从PC12细胞释放乳酸脱氢酶外,PF还显着减轻了H2O2诱导的细胞活力降低。另外,在PF处理的细胞中,与凋亡相关的核因子(NF)-κB的激活受到抑制,并且肿瘤坏死因子α和白介素(IL)-1β的表达水平降低。总之,本研究表明,PF能够通过阻断神经炎性因子NF-κB的活化来降低H2O2诱导的毒性。这些结果表明PF可能是用于治疗神经系统疾病和损伤的有价值的神经保护剂。

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