Effectiveness of acupuncture therapy for postherpetic neuralgia: an umbrella review protocol.

INTRODUCTION: Several systematic reviews and meta-analysis indicate that acupuncture and related therapies may be a valuable adjunctive technique to pharmacological interventions for pain management of postherpetic neuralgia (PHN). However, the robustness of the results of these studies has not been evaluated. The aim of this proposed umbrella review is to provide more reliable evidence of the effectiveness of acupuncture therapy for PHN based on medical references for healthcare decision makers. METHODS AND ANALYSIS: PubMed, EMBASE, The Cochrane Library, Web of Science, Chinese BioMedical Literature Database, VIP Database for Chinese Technical Periodicals, China National Knowledge Infrastructure and Wan fang Database will be used to retrieve reviews. The time of publication will be limited from inception to March 2021. Two reviewers will screen all retrieved articles independently to identify their eligibility and extract the data. The quality will be assessed independently by two trained reviewers using Assessment of Multiple Systematic Reviews-2 for methodological quality, Risk of Bias in Systematic Review for level of bias, Preferred Reporting Items for Systematic Reviews and Meta-Analysis for reporting quality and Grading of Recommendations Assessment, Development and Evaluation for the quality of evidence. Any disagreements will be settled by discussion or the involvement of a third reviewer. ETHICS AND DISSEMINATION: The protocol of this review does not require ethical approval because the research will be based on publicly available data. The findings will be disseminated through publication in peer-reviewed international journals or presentation in academic conference. PROSPERO REGISTRATION NUMBER: CRD42020173341. REPORTING CHECKLIST: PRISMA-P, 2015.

[Therapeutic effect and mechanism of silver needle heat conduction therapy combined with loxoprofen sodium patch in patients with knee osteoarthritis].

OBJECTIVE: To observe the clinical efficacy of silver needle heat conduction therapy combined with loxoprofen sodium patch in the treatment of knee osteoarthritis (KOA). METHODS: A total of ninety-two patients with KOA were randomly and equally divided into loxoprofen sodium group and silver needle heat conduction therapy + loxoprofen sodium (combination) group, with 46 cases in each group. Patients of the combination group were treated with silver needle heat conduction therapy combined with loxoprofen sodium patch, while those of the loxoprofen sodium group were treated with loxoprofen sodium patch. The treatment was conducted for 4 weeks. The Western Ontario McMaster Universities Osteoarthritis Index (WOMAC), bone metabolism index ï¼»including bone gla protein (BGP), bone-specific alkaline phosphatase (BALP), tartrate resistant acid phosphatase isomer (TRACP)-5bï¼½, and inflammation factors ï¼»including the tumor necrosis factor-α (TNF-α), transforming growth factor-ß (TGF-ß), interleukin-1ß (IL-1ß)ï¼½ were observed before and after treatment. The therapeutic effect was assessed after the treatment. RESULTS: After the treatment, the total scores of WOMAC, the levels of serum TRACP-5b, TNF-α and IL-1ß were significantly decreased (P<0.01), while the levels of serum BGP, BALP, and TGF-ß were significantly increased (P<0.01) in the two groups compared with their own pre-treatment. Silver needle plus loxoprofen sodium was more effective in reducing WOMAC score, TRACP-5b, TNF-α, IL-1ß level (P<0.01), and up-regulating BGP, BALP, and TGF-ß level (P<0.01) than loxoprofen. Of the 46 cases in the loxoprofen sodium and combination groups, 33 and 41 were effective, with the effective rate being 71.7% and 89.1%, respectively. The comprehensive therapeutic effect of the combination group was significantly superior to that of the loxoprofen group (P<0.05). CONCLUSION: Silver needle heat conduction therapy combined with loxoprofen sodium can effectively treat KOA, its mechanism may be related to alleviating inflammation and improving bone metabolism.

Phosphatidylinositol 3-kinase mediates pain behaviors induced by activation of peripheral ephrinBs/EphBs signaling in mice.

EphBs receptors and their ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Our recent evidence has shown that ephrinBs acted as a sensitizer to participate in peripheral sensitization and hyperalgesia induced by activation of peripheral ephrinBs/EphBs signaling. In the present study, we explored the role of phosphatidylinositol 3-kinase (PI3K) in ephrinB1-Fc-induced pain behaviors. Intraplantar injection of ephrinB1-Fc produced a time- and dose-dependent increase of PI3K-p110gamma expression and of phosphorylation of AKT in skin of injection site. Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of peripheral AKT by ephrinB1-Fc. The activated AKT expressed in peripheral nerve terminals and DRG peptide-containing and small non-peptide-containing neurons. Inhibition of peripheral PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal Fos protein expression induced by intraplantar injection of ephrinB1-Fc. Furthermore, pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented ephrinB1-Fc-induced ERK activation in a dose-dependent manner. These data demonstrated that PI3K and PI3K crosstalk to ERK signaling mediated pain behaviors induced by activation of peripheral ephrinBs/EphBs signaling in mice.

Activation of peripheral ephrinBs/EphBs signaling induces hyperalgesia through a MAPKs-mediated mechanism in mice.

EphBs receptors and ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Ours and other studies have demonstrated that spinal ephrinBs/EphBs signaling was involved in the modulation of nociceptive information and central sensitization. However, the role of ephrinBs/EphBs signaling in peripheral sensitization is poorly understood. This study shows that intraplantar (i.pl.) injection of ephrinB1-Fc produces a dose- and time-dependent thermal and mechanical hyperalgesia and the increase of spinal Fos protein expression in mice, which can be partially prevented by pre-treatment with EphB1-Fc. EphrinB1-Fc-induced hyperalgesia is accompanied with the NMDA receptor-mediated increase of expression in peripheral and spinal phosphorylated mitogen-activated protein kinases (phospho-MAPKs) including p-p38, pERK and pJNK, and also is prevented or reversed by the inhibition of peripheral and spinal MAPKs. Furthermore, in formalin inflammation pain model, pre-inhibition of EphBs receptors by the injection of EphB1-Fc reduces pain behavior, which is accompanied by the decreased expression of peripheral p-p38, pERK and pJNK. These data provide evidence that ephrinBs may act as a prominent contributor to peripheral sensitization, and demonstrate that activation of peripheral ephrinBs/EphBs system induces hyperalgesia through a MAPKs-mediated mechanism.