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Objectives: To observe the effect of the acupuncture of myofascial trigger points (MTrPs) in the treatment of lower extremity varicose veins (LEVVs). Methods: Overall, 260 patients with LEVVs participated in this study. LEVVs were selected based on diagnostic criteria of Clinical, Etiology, Anatomy, and Pathophysiology levels 2–5 and classified into six types on the basis of their anatomical positions. The MTrPs in the lower extremities were localized in accordance with the classification of LEVVs and treated by MTrPs acupuncture combined with self-massage and self-stretching. The interval between each treatment was 2 weeks to 1 month, depending on needling pain tolerance of each patient. An in-house evaluation was used to estimate the proportion of varicose veins in the lower limbs and their accompanying symptoms. The treatment effect was evaluated before each treatment and at 1-year follow-up. Results: The mean evaluation score of LEVVs before the treatment course was 3.66 ± 1.19. After the course, this reduced to 1.18 ± 0.97, with the following response rates: 85% for excellent and good and 15% for medium. After 1-year follow-up, the mean evaluation score of all patients was 1.11 ± 0.92, with the following response rates: 87% for excellent and good, and 13% for medium. Conclusions: In some patients, MTrP acupuncture could cure LEVVs and its accompanying symptoms. These LEVVs are probably caused by fascia tension as a pre-pathology induced by the MTrPs. [ABSTRACT FROM AUTHOR]

• Abnormal endplate noise, including positive neurons, fibrillation potentials, fasciculation potential, and endplate spikes are present at MTrSs. • This study shows for the first time the morphological nodular features of MTrSs, which are located at the motor endplates, through AChE staining. • Excessive ACh release and decreased AChE activity at MTrSs stimulated muscle action potential and muscle contraction. Myofascial trigger points (MTrPs) are defined as hyperirritable spots in a palpable taut band (TB) of skeletal muscle fibers. Knowing the formation and location of MTrPs is a great help to prevent their development and inactivate existing MTrPs. This study aimed to obtain new evidence that myofascial trigger spots (MTrSs), which are similar to human MTrPs, are found in dysfunctional motor endplates by observing the morphological characteristics of muscles and changes in biochemical substances. A total of 32 male Sprague Dawley rats were randomly divided into four groups: two control groups (i.e., C1 and C2) and two model groups (i.e., M1 and M2). C1 and M1 were used for acetylcholine (ACh) content measurement, while C2 and M2 were utilized for acetylcholinesterase (AChE) staining. In the model groups, blunt striking injury was induced and eccentric exercise was applied to the left gastrocnemius for 8 weeks. After 1 month, spontaneous electrical activity(SEA), AChE optical density (OD), muscle fiber diameter, and ACh content were measured. The results showed that extensive abnormal endplate noise (aEPN), including positive neurons, fibrillation potentials, fasciculation potential, and high amplitude (endplate spikes [EPS]), is present at MTrSs in M1. Quantitative electromyography results showed that the amplitudes of aEPN and frequency of EPS in M1 were significantly higher than those of C1. The ACh content of MTrSs in M1 was significantly higher than that in C1. The AChE OD value of M2 was significantly lower than that of C2. In addition, the diameter of the muscle fibers in the AChE-stained area was longer in M2 than in C2. In conclusion, MTrSs formed at the motor endplate with a larger diameter of muscle fibers. Excessive ACh release and decreased AChE activity at MTrSs stimulated muscle action potential and muscle contraction. [ABSTRACT FROM AUTHOR]

Objective. The aims of this study are to investigate the changes in spontaneous electrical activities (SEAs) and in acetylcholine (ACh), acetylcholine receptor (AChR), and acetylcholine esterase (AChE) levels after dry needling at myofascial trigger spots in model rats. Materials and Methods. Forty-eight male Sprague-Dawley rats were divided into four groups. Thirty-six rats were assigned to three model groups, which underwent MTrSs modeling intervention. Twelve rats were assigned to the blank control (BC) group. After model construction, the 36 model rats were randomly subdivided into three groups according to treatment: MTrSs model control (MC) and two dry needling groups. One dry needling group received puncturing at MTrSs (DN-M), whereas the other underwent puncturing at non-MTrSs (DN-nM). Dry needling treatment will last for two weeks, once a week. SEAs and ACh, AChR, and AChE levels were measured after one-week rest of dry needling treatment. Results. The amplitudes and frequencies of endplate noise (EPN) and endplate spike (EPS) significantly decreased after dry needling treatment in the DN-M group. Moreover, ACh and AChR levels significantly decreased, whereas AChE significantly increased after dry needling treatment in the DN-M group. Conclusion. Dry needling at the exact MTrSs is more effective than dry needling at non-MTrSs. [ABSTRACT FROM AUTHOR]

Highlights • miR-381 was decreased in CCI rats, and overexpression of miR-381 depressed neuroinflammation. • HMGB1 and CXCR4 were predicted as downstream targets of miR-381 and miR-381 modulated HMGB1 and CXCR4 expression negatively. • miR-381 might act as a potential therapeutic target for neuropathic pain development. Abstract MicroRNA are significant regulators of neuropathic pain development. Neuroinflammation contributes a lot to the progression of neuropathic pain. miR-381 is involved in various pathological processes. However, the role of miR-381 in neuropathic pain development remains barely understood. Therefore, in our study, we aimed to investigate the effects of miR-381 on the process of neuropathic pain progression by establishing a rat model using chronic sciatic nerve injury (CCI). Here, we observed that miR-381 was dramatically decreased in CCI rats. Up-regulation of miR-381 strongly reduced neuropathic pain behaviors including mechanical and thermal hyperalgesia. In addition, inflammatory cytokine expression, including IL-6, IL-10 and TNF-α were significantly repressed by overexpression of miR-381. High mobility group box 1 protein (HMGB1) and Chemokine CXC receptor 4 (CXCR4) participate in neuropathic pain development. In our present study, HMGB1 and CXCR4 were predicted as direct targets of miR-381 by employing bioinformatics analysis. Overexpression of miR-381 was able to restrain the expression of HMGB1 and CXCR4 greatly. The direct correlation between HMGB1 and CXCR4 and miR-381 was confirmed in our research. Furthermore, we found that HMGB1 and CXCR4 were increased in CCI rats time-dependently. Moreover, it was demonstrated that silence of HMGB1 and CXCR4 in CCI rats depressed neuropathic pain progression greatly. In conclusion, it was indicated that miR-381could inhibit neuropathic pain development through targeting HMGB1 and CXCR4. [ABSTRACT FROM AUTHOR]