Effects of chlorogenic acid on voltage-gated potassium channels of trigeminal ganglion neurons in an inflammatory environment

• K+ channels are potential therapeutic targets for trigeminal inflammatory pain.
• CGA antagonized the effects of PGE2 on the subtypes of K+ channels on TGNs.
• Mechanisms of CGA analgesia derived from its different behaviors on IK,Aand IK,V.

Chlorogenic acid (CGA) composed of coffee acid and quinic acid is an effective ingredient of many foods and medicines and widely exhibits biological effects. Recently, it is reported to have analgesic effect. However, little is known about the analgesic mechanism of CGA. In this study, whole-cell patch-clamp recordings were performed on two main subtypes (IK,A and IK,V channels) of voltage-gated potassium (KV) channels in small-diameter(<30 μm) trigemianl ganglion neurons to analyze the effects of CGA in an inflammatory environment created by Prostaglandin E2 (PGE2). On one hand, the activation and inactivation V1/2 values of IK,A and IK,V channels showed an elevation towards a depolarizing shift caused by PGE2. On the other hand, the activation and inactivation V1/2 values of the two channels had a reduction towards a hyperpolarizing shift caused by CGA under PGE2 pretreatment. Our results demonstrated that CGA may exhibited an analgesic effect by promoting KV channels activation and inactivation under inflammatory condition, which provided a novel molecular and ionic mechanism underlying anti-inflammatory pain of CGA.