Medical Research

Electroacupuncture at Ipsilateral or Contralateral ST36-ST37 Acupoints on Inflammatory Pain.

Kristen Sparrow • February 09, 2017

Modern innovations for acupuncture
Ancient Medicine Made Modern

Patients often wonder why I treat both sides (Right and Left) in musculoskeletal conditions.  This has long been a trick in Chinese Medicine, particularly if the inflamed joint is very sensitive, or in a cast and it often works great.  The study below shows, perhaps, why.  It’s overall reduction in inflammatory activity.

Sci Rep. 2016 Feb 24;6:22123. doi: 10.1038/srep22123.

Probing the Effects and Mechanisms of Electroacupuncture at Ipsilateral or Contralateral ST36-ST37 Acupoints on CFA-induced Inflammatory Pain.

Lu KW1,2, Hsu CK3,4,5, Hsieh CL2,6, Yang J2, Lin YW3,7.


Transient receptor potential vanilloid 1 (TRPV1) and associated signaling pathways have been reported to be increased in inflammatory pain signaling. There are accumulating evidences surrounding the therapeutic effect of electroacupuncture (EA). EA can reliably attenuate the increase of TRPV1 in mouse inflammatory pain models with unclear signaling mechanisms. Moreover, the difference in the clinical therapeutic effects between using the contralateral and ipsilateral acupoints has been rarely studied. We found that inflammatory pain, which was induced by injecting the complete Freund’s adjuvant (CFA), (2.14 ± 0.1, p < 0.05, n = 8) can be alleviated after EA treatment at either ipsilateral (3.91 ± 0.21, p < 0.05, n = 8) or contralateral acupoints (3.79 ± 0.25, p < 0.05, n = 8). EA may also reduce nociceptive Nav sodium currents in dorsal root ganglion (DRG) neurons. The expression of TRPV1 and associated signaling pathways notably increased after the CFA injection; this expression can be further attenuated significantly in EA treatment. TRPV1 and associated signaling pathways can be prevented in TRPV1 knockout mice, suggesting that TRPV1 knockout mice are resistant to inflammatory pain. Through this study, we have increased the understanding of the mechanism that both ipsilateral and contralateral EA might alter TRPV1 and associated signaling pathways to reduce inflammatory pain.