No abstract

Acupuncture can effectively improve the sleep state, and most PD patients have sleep disorders. In this study, we used acupuncture to intervene in the sleep state of PDSD, so as to observe the changes and dose effect of Acutreatment on PDSD. 57 patients with PDSD, during medical treatment, aged 40–70 years were recruited to enroll in this trial. Each participant completed one condition, namely, Acutreatment ( n = 30 ) and sham Acutreatment (placebo, stick flat needle on skin, n = 27 ). The Acutreatment was applied for 30 min once a day for a 30-day observation. UPDRSIII scores for motor symptom assessment and sleeping quality were assessed by PDSS-2, ESS as well as ActiGraph. Scale evaluation was made on the first day of admission and the thirtieth day. There were significant differences on all outcome indicators, except UPDRSIII, on day 30 compared with day 1 ( P < 0.01 ). Compared with sham Acutreatment therapy, Acutreatment therapy has better performance in sleep latency, total sleep time, and sleep efficiency ( P < 0.01 ). ActiGraph indicated that sleep efficiency of sham or Acutreatment in day 6 was significantly lower than that in day 5 ( P < 0.05 and P < 0.01 ) and Acutreatment in day 7 was significantly lower than that in day 6 ( P < 0.01 ). The sleep efficiency of Acutreatment in days 5, 6, and 7 was significantly higher than that in sham Acutreatment ( P < 0.01 ). Moreover, Acutreatment in days 26, 27, and 28 was significantly higher than that in sham Acutreatment ( P < 0.01 ). There was a close correlation between the difference of UPDRSIII and PDSS-2 ( r = 0.5090 , P < 0.05 ), sleep latency ( r = 0.7201 , P < 0.01 ), TST ( r = − 0.6136 , P < 0.01 ), and sleep efficiency ( r = − 0.6707 , P < 0.01 ). The sleep condition of PDSD patients can be improved by acupuncture, which can effectively relieve sleep quality, can also be shown by ActiGraph, and shows a dose-response relationship. Future research should explore Acutreatment with a larger sample size and compare the Acutreatment protocol goal formation of the system scheme.

To study the role of adenosine A2A receptor (A2AR) in mediating the anti-inflammatory effect of electroacupuncture (EA) on synovitis in collagen-induced arthritis (CIA), C57BL/6 mice were divided into five treatment groups: Sham-control, CIA-control, CIA-EA, CIA-SCH58261 (A2AR antagonist), and CIA-EA-SCH58261. All mice except those in the Sham-control group were immunized with collagen II for arthritis induction. EA treatment was administered using the stomach 36 and spleen 6 points, and stimulated with a continuous rectangular wave for 30 min daily. EA treatment and SCH58261 were administered daily from days 35 to 49 (n = 10). After treatment, X-ray radiography of joint bone morphology was established at day 60 and mouse blood was collected for ELISA determination of tumor necrosis factor alpha (TNF-α) levels. Mice were sacrificed and processed for histological examination of pathological changes of joint tissue, including hematoxylin-eosin staining and immunohistochemistry of A2AR expression. EA treatment resulted in significantly reduced pathological scores, TNF-α concentrations, and bone damage X-ray scores. Importantly, the anti-inflammatory and tissue-protective effect of EA treatment was reversed by coadministration of SCH58261. Thus, EA treatment exerts an anti-inflammatory effect resulting in significant protection of cartilage by activation of A2AR in the synovial tissue of CIA.

Transcutaneous acupoint electrical stimulation shows potential as an adjunct to conventional pain treatment following surgical abortion in nulliparae.

Background: Recently, the role of electroacupuncture (EA) in chronic neuropathic pain has been widely reported. However, its specific mechanisms and ability to mitigate depression-like behaviors induced by chronic pain remains unclear. This study aims to determine the analgesic and antidepressant effect of EA.Methods: The mechanical threshold sensory and hot plate tests were employed to measure mechanical hyperalgesia and thermal allodynia. The open filed test (OFT) and tail suspension test (TST) were used to observe depressive behavior in chronic constrictive injury (CCI) mice. In addition, the 5-hydroxytryptamine(5-HT) and brain-derived neuropathic factor (BDNF) levels in the anterior cingulate cortex (ACC) and spinal cord were assessed using enzyme-linked immunosorbent assay (ELISA). The protein levels of cAMPresponse element-binding protein (CREB) and BDNF in the ACC were analyzed by western blotting.Results: Our results demonstrated that EA treatment could increase the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) values. Also, EA improved the CCI-induced depression-like behaviors, and significantly reversed the down-regulation of BDNF and 5-HT expression in the ACC and spinal cord after CCI. Furthermore, EA regulated the level of CREB in the ACCs and spinal cords of mice.Conclusions: These results suggested that the analgesic and antidepressant effect of EA is achieved through regulating CREB-5-HT/BDNF signaling pathway in the ACCs and spinal cords of mice.