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

Abstract

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.