Objective To observe the changes of cardiovascular function after acupuncture at Neiguan (PC 6) respectively with slowly twirling needling and tube needling in healthy subjects, and to objectively evaluate the pain intensity of the two needling methods.Method A hundred healthy young subjects were randomized into group A and group B, 50 cases in each group. Neiguan (PC 6) point was selected for acupuncture in both groups. In the first stage, group A received acupuncture by slowly twirling needling, while group B received acupuncture with tube needling; in the second stage (a week later), group A received acupuncture with tube needling, while group B by slowly twirling needling. The Short-form McGill Pain Questionnaire (SF-MPQ) was observed after acupuncture for each subject, and ZXG-E automatic cardiovascular function detector was adopted to evaluate the cardiovascular function before puncturing, 5 min after puncturing, and 30 min after puncturing.Result The Sensory Pain Rating Index (S-PRI) and total SF-MPQ scores of slowly twirling needling were significantly different from that of tube needling (P<0.01). The Affective Pain Rating Index (A-PRI), Visual Analogue Scale (VAS), and Present Pain Intensity (PPI) of slowly twirling needling method were significantly different from that of tube needling (P<0.01). At 5 min after needle insertion, the FEK and VER values of twirling needling were significantly different from that of tube needling (P<0.01).Conclusion The pain produced by slowly twirling needling is more variant and stronger than that by tube needling, and this pain variation can produce a positive effect on cardiovascular function.

Alzheimer's disease (AD) is a leading cause of dementia in the elderly. Mitogen-activated protein kinase phosphatase 1 (MKP-1) plays a neuroprotective role in AD. However, the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, thereby repressing mRNA translation. Here, we reported that the microRNA-429-3p (miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2A^APP AD model cells. We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3'-untranslated region (3' UTR). Inhibition of miR-429-3p by its antagomir (A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation. More importantly, intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase (ERK1/2)-mediated GluA1 hyperphosphorylation at Ser831 site, thereby increasing the surface expression of GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Together, these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice, suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.