Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke

Life Sci. 2016 Apr 15:151:313-322. doi: 10.1016/j.lfs.2016.01.045. Epub 2016 Mar 14.

Abstract

Aims: Electroacupuncture (EA) is one of the safety and effective therapies for improving neurological and sensorimotor impairment via blockade of inappropriate inflammatory responses. However, the mechanisms of anti-inflammation involved is far from been fully elucidated.

Main methods: Focal cerebral ischemic stroke was administered by the middle cerebral artery occlusion and reperfusion (MCAO/R) surgery. The MCAO/R rats were accepted EA treatment at the LI 11 and ST 36 acupoints for consecutive 3days. The neurological outcome, animal behaviors test and molecular biology assays were used to evaluate the MCAO/R model and therapeutic effect of EA.

Key findings: EA treatment for MCAO rats showed a significant reduction in the infarct volumes accompanied by functional recovery in mNSS outcomes, motor function performances. The possible mechanisms that EA treatment attenuated the over-activation of Iba-1 and ED1 positive microglia in the peri-infract sensorimotor cortex. Simultaneously, both tissue and serum protein levels of the tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were decreased by EA treatment in MCAO/R injured rats. The levels of inflammatory cytokine tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) were decreased in the peri-infract sensorimotor cortex and blood serum of MCAO/R injured rats after EA treatment. Furthermore, we found that EA treatment prevented from the nucleus translocation of NF-κB p65 and suppressed the expression of p38 mitogen-activated protein kinase (p38 MAPK) and myeloid differentiation factor 88 (MyD88) in the peri-infract sensorimotor cortex.

Significance: The findings from this study indicated that EA improved the motor impairment via inhibition of microglia-mediated neuroinflammation that invoked NF-κB p65, p38 MAPK and MyD88 produced proinflammatory cytokine in the peri-infract sensorimotor cortex of rats following ischemic stroke.

Keywords: Electroacupuncture; Ischemic stroke; Microglia; Motor impairment; Neuroinflammation.

MeSH terms

  • Animals
  • Brain Infarction / pathology
  • Brain Ischemia / complications
  • Brain Ischemia / metabolism*
  • Electroacupuncture*
  • Infarction, Middle Cerebral Artery
  • Inflammation / metabolism*
  • Interleukin-1beta / blood
  • Interleukin-1beta / metabolism
  • Interleukin-6 / blood
  • Interleukin-6 / metabolism
  • Male
  • Microglia / metabolism*
  • Motor Disorders / therapy*
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / metabolism
  • Rats
  • Reperfusion Injury / metabolism
  • Sensorimotor Cortex / pathology*
  • Stroke / complications
  • Stroke / metabolism*
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Interleukin-1beta
  • Interleukin-6
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • p38 Mitogen-Activated Protein Kinases