Effect of MLC901 on MIR30C–5P expression, TGF-Β expression, VEGF receptor expression, degree of axon demyelination and changes in neuropathic pain behaviour in experimental animals experiencing neuropathic pain with circumferential spinal stenosis method

Abstract

Neuropathic pain is a major problem whose pathogenesis is not known yet, which makes it difficult to treat. Effective treatment of neuropathic pain usually uses multimodal therapy that takes a long time but causes major health problems, which are commonly found in women over 50 years of age and are generally caused by lumbar radiculopathy due to lumbar spinal stenosis. The narrowing of the spinal canal resembles an ischemic condition that can increase the expression of VEGF in the dorsal root ganglion and then result in shortened walking distance (intermittent claudication). The effect of VEGF is thought to be through binding to VEGFR1 and VEGFR2, whose levels are increased in conditions of hyperalgesia and neuropathic pain. Immune mechanisms play a role in the pathogenesis of neuropathic pain, through the balanced process of pro-inflammatory cytokines and anti-inflammatory cytokines, TGF-β, which are immunosuppressive. MLC901 is a simplified traditional medicine formula from MLC601, which affects the nervous system through three main mechanisms, namely neuroprotection, neuro-regeneration and neuro-restoration. Elevated levels of MLC901 promote angiogenesis. This review discusses the effect of MLC901 on miR30c-5p expression, TGF-β expression, VEGF receptor expression, degree of axon demyelination and changes in neuropathic pain behaviour in experimental animals experiencing neuropathic pain using the circumferential spinal stenosis method. These findings may provide new targets for further scientific research on the molecular mechanisms of neuropathic pain and potential therapeutic interventions.

Access to Document

Other files and links

• Link to publication in Scopus
• Open Access Version Available

Fingerprint