The analgesic effect of paeoniflorin: A focused review

Abstract

Pain has been a prominent medical concern since ancient times. Despite significant advances in the diagnosis and treatment of pain in contemporary medicine, there is no a therapeutic cure for chronic pain. Chinese herbaceous peony, a traditional Chinese analgesic herb has been in clinical use for millennia, with widespread application and substantial efficacy. Paeoniflorin (PF), the main active ingredient of Chinese herbaceous peony, has antioxidant, anti-inflammatory, anticancer, analgesic, and antispasmodic properties, among others. The analgesic effect of PF, involving multiple critical targets and pain regulatory pathways, has been a hot spot for current research. This article reviews the literature related to the analgesic effect of PF in the past decade and discusses the molecular mechanism of the analgesic effect of PF, including the protective effects of nerve cells, inhibition of inflammatory reactions, antioxidant effects, reduction of excitability in nociceptor, inhibition of the nociceptive excitatory neuroreceptor system, activation of the nociceptive inhibitory neuroreceptor system and regulation of other receptors involved in nociceptive sensitization. Thus, providing a theoretical basis for pain prevention and treatment research. Furthermore, the prospect of PF-based drug development is presented to propose new ideas for clinical analgesic therapy.

Keywords: analgesic effect; molecular mechanism; monomer of Chinese traditional herbs; paeoniflorin.

Figure 1

PF induces analgesia by downregulating glutamate levels in ACC and decreasing ERK expression in DRG. Note: PF: paeoniflorin; ACC: anterior cingulate cortex; DRG: dorsal root ganglion; ERK: extracellular signal-regulated kinase. PGE: prostaglandin E; NMDA: N-methyl-d-aspartic; β-EP: β-Endorphin; CCL2: chemokine ligand 2.

Figure 2

The analgesic effect of PF is mediated through the regulation of MAPK and upstream inflammatory factors. Note: MAPK: mitogen-activated protein kinases; NF-κB: nuclear transcription factor-κB; ASK1: apoptosis signal-regulated kinase 1; p-ERK: p-extracellular signal-regulated kinase; p-p38: phosphorylated-p38; p-JNK: phosphorylated c-jun N-terminal kinase; MMP9: metalloproteinase-9; c-FOS: protooncogene; TNF-α: tumor necrotic factor-α; IL-1β/IL-1: interleukin-1; IL-6: interleukin-6.