Emodin ameliorates diabetic neuropathic pain through inhibiting up-regulation of TRPV1 and pro-inflammatory cytokines in dorsal root ganglions in rats

ABSTRACT

@#Background & Objective: Peripheral neuropathy is one of the most common complications of diabetes and leads to sensory symptoms, including diabetic neuropathic pain (DNP). Emodin has potential analgesic effect for the treatment of pain-related diseases. However, the analgesic effect of emodin on DNP and its possible mechanism remains unknown. The aim of the present study is to investigate the effect of emodin on STZ-induced DNP in rats and its potential molecular mechanism. Methods: To determine the analgesic effect of emodin on DNP, a mouse model of STZ-induced DNP was established. The pain-related behaviors were evaluated by von Frey test, and hot plate test. The mRNA and protein expression of several TRP channels was detected by qRT-PCR and western blot methods, and the level of inflammatory cytokines was determined by ELISA. Results: The mechanical and thermal pain thresholds were significantly decreased in DNP rats. A single injection of emodin treatment significantly reduced DNP. Further results demonstrated that emodin inhibited the up-regulation of Trpv1 mRNA in the DRG of DNP rats. Our data also indicated that emodin significantly reduced the levels of TNF-α, IL-1β and IL-6 in the DRG of DNP rats. Conclusions: Emodin ameliorates mechanical allodynia and thermal hyperalgesia in DNP rats by down-regulating the expression of TRPV1 in DRG and the expression of TNF-α, IL-1β and IL-6. Emodin serves as a potent analgesic reagent for treatment and prevention of DNP.