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

Abstract

Abstract. Paeoniflorin (PF) is a product derived fromPaeoniae 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 (H 2 O 2 )-induced apoptosis in PC12 cells, to improve the understanding of the mechanisms underlying its neuroprotective properties. The H 2 O 2 -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 H 2 O 2 -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 H 2 O 2 -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.

The effects of paeoniflorin injection on soluble triggering receptor expressed on myeloid-1 (sTREM-1) levels in severe septic rats

“…PAE was also able to inhibit the activation of the neuro-inflammatory factor NF-κB thereby alleviating H 2 O 2 -induced oxidative stress [26]. In the present study, we found that PAE, the most abundant component in XBJ injection [22], significantly inhibited the plasma sTREM-1 level in rats of endotoxin-induced sepsis.…”

“…In a transgenic mouse model of Alzheimer's disease, PAE attenuated amyloidogenesis and the inflammatory responses [25]. Its neuroprotective effect was also reported in rat cells, where PAE reduced H 2 O 2 -induced toxicity by blocking the activation of the neuro-inflammatory factor NF-κB [26]. Moreover in rats, PAE ameliorated ANIT-induced cholestasis by activating Nrf2 through an PI3K/Akt-dependent pathway [27], and improved regional cerebral blood flow and suppressed inflammatory factors in the hippocampus of rats with vascular dementia [28].…”

Daily administration of yokukansan and keishito prevents social isolation-induced behavioral abnormalities and down-regulation of phosphorylation of neuroplasticity-related signaling molecules in mice

“…This mechanism is very likely to be implicated in the effect of KST, since KST ameliorated ISO-induced behavioral deficits when the administration was started from week 0, but not from week 2 after starting ISO. Moreover, chemical constituents of YKS and KST have been reported to have neuroprotective effects [33–36], suggesting that these compounds protect central cholinergic systems from ISO-induced dysfunction. This hypothesis is currently under investigation in our laboratory.…”

Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway

“…Paeoniflorin, a major pharmacological pinane monoterpene glucoside, was first isolated from the Ranunculaceae plant in 1963. It is widely accepted that paeoniflorin has antioxidant, anti-inflammation, hepatoprotective and neuroprotective effects (4)(5)(6)(7). In an adjuvant-induced arthritis model, paeoniflorin inhibited the expression of IL-1β, IL-6, IL-17, and TNF-α and upregulated the production of TGF-β1 (8).…”