Electroacupuncture-Like Stimulation at the Baihui (GV20) and Dazhui (GV14) Acupoints Protects Rats against Subacute-Phase Cerebral Ischemia-Reperfusion Injuries by Reducing S100B-Mediated Neurotoxicity

Abstract

ObjectivesThe purpose of this study was to evaluate the effects of electroacupuncture-like stimulation at the Baihui (GV20) and Dazhui (GV14) acupoints (EA at acupoints) during the subacute phase of cerebral ischemia-reperfusion (I/R) injury and to establish the neuroprotective mechanisms involved in the modulation of the S100B-mediated signaling pathway.MethodsThe experimental rats were subjected to middle cerebral artery occlusion (MCAo) for 15 min followed by 1 d or 7 d of reperfusion. EA at acupoints was applied 1 d postreperfusion then once daily for 6 consecutive days.ResultsWe observed that 15 min of MCAo caused delayed infarct expansion 7 d after reperfusion. EA at acupoints significantly reduced the cerebral infarct and neurological deficit scores. EA at acupoints also downregulated the expression of the glial fibrillary acidic protein (GFAP), S100B, nuclear factor-κB (NF-κB; p50), and tumor necrosis factor-α (TNF-α), and reduced the level of inducible nitric oxide synthase (iNOS) and apoptosis in the ischemic cortical penumbra 7 d after reperfusion. Western blot analysis showed that EA at acupoints significantly downregulated the cytosolic expression of phospho-p38 MAP kinase (p-p38 MAP kinase), tumor necrosis factor receptor type 1-associated death domain (TRADD), Fas-associated death domain (FADD), cleaved caspase-8, and cleaved caspase-3 in the ischemic cortical penumbra 7 d after reperfusion. EA at acupoints significantly reduced the numbers of GFAP/S100B and S100B/nitrotyrosine double-labeled cells.ConclusionOur study results indicate that EA at acupoints initiated 1 d postreperfusion effectively downregulates astrocytic S100B expression to provide neuroprotection against delayed infarct expansion by modulating p38 MAP kinase-mediated NF-κB expression. These effects subsequently reduce oxidative/nitrative stress and inhibit the TNF-α/TRADD/FADD/cleaved caspase-8/cleaved caspase-3 apoptotic pathway in the ischemic cortical penumbra 7 d after reperfusion.

Neuroinflammatory response to experimental stroke is inhibited by eriodictyol

“…MCAO induces a significant increase in NF-kB, which in turn mediates the transcription of mRNA and an increase in TNF-α expression up to 7 days after the ischemic event [72]. iNOS synthesizes large amounts of NO (nitric oxide).…”

The Apoptosis Regulation Mechanisms in Hypothalamic Neurons in Physiological and Pathological (Overexpression of Oncogene HER-2/Neu) Aging

“…Similar changes have been shown to be associated with cell transformation and cancer development [3,12,13]. In addition, the absence of pin1 affects embryonic fibroblasts, leading to rapid genomic instability and the so-called immortality due to inactivation of p53 and further to aggressive transformation and carcinogenesis [16].…”

Early electroacupuncture treatment ameliorates neuroinflammation in rats with traumatic brain injury

“…They found that TNF-α expression was lower in the EA group than in the model and sham-operated groups [7]. In a study by Cheng et al, acupuncture at the Baihui (GV 20) and Dazhui (GV14) acupoints significantly downregulated the expression of TNF-α, GFAP, S100B, and nuclear factor-kB in the ischemic cortical penumbra [8]. Jiang et al selected Shuigou (GV 26) and Fengfu (DU16) for acupuncture treatment of traumatic spinal cord injury and found that EA had anti-oxidative, anti-inflammatory, and anti-apoptotic effects as indicated by reduced expression of inflammatory cytokines, including TNF- α [9].…”

“…Previous studies have demonstrated the beneficial effects of EA on stroke [6–8], spinal cord injury [9], arthritis [10], and sciatica [11]. Recently, we have demonstrated that application of EA 60 min post-TBI has neuroprotective effects on neuronal cells.…”