Electroacupuncture ameliorates disuse muscular atrophy and inhibits the NLRP3 inflammasome and SIRT1 through miR-133a in a mouse model.

["Jiaji" (EX-B2) electroacupuncture modulates NLRP3 inflammasome activation to improve limb dysfunction in amyotrophic lateral sclerosis mice].

[Effects of electroacupuncture on motor function and PGC-1α/FNDC5/BDNF pathway in muscle and brain of SAMP8 mice].

Electroacupuncture-mediated lncRNA TUG1 regulates the miR-127-3p/NF-κB p65 axis to inhibit IBS-D low-grade intestinal inflammation

Background Electroacupuncture (EA) demonstrates efficacy in alleviating diarrhea-predominant irritable bowel syndrome (IBS-D), yet its mechanisms concerning low-grade intestinal inflammation remain insufficiently elucidated. This study investigated whether EA ameliorates IBS-D symptoms by modulating the long non-coding RNA Taurine Upregulated Gene 1 (lncRNA TUG1)/microRNA-127 -3p (miR-127-3p)/nuclear factor-kappa B p65 (NF-κB p65) axis. Methods An IBS-D rat model was established using maternal separation, acetic acid enema, and chronic restraint stress. Rats were randomly allocated into control, model, EA (at ST-25 and ST-37), drug (rifaximin), and PDTC (NF-κB p65 inhibitor) groups. Behavioral assessments (body weight, loose stool rate, abdominal withdrawal reflex) were conducted. Molecular analyses included dual-luciferase reporter assays, RT-qPCR, western blot, ELISA, and immunofluorescence to evaluate the TUG1/miR-127-3p/NF-κB p65 axis, inflammatory factors (TNF-α, NLRP3, IL-6), and tight junction proteins (occludin, claudin-1, ZO-1). Intestinal ultrastructure was examined by electron microscopy. Results EA significantly improved general status, reduced diarrhea and visceral hypersensitivity in IBS-D rats, comparable to rifaximin and PDTC. Mechanistically, EA upregulated colonic lncRNA TUG1 expression, which sequesters miR-127-3p and partially derepresses NF-κB negative regulators (IκBα, A20), consistent with attenuated NF-κB pathway activation. This was associated with downregulated downstream pro-inflammatory mediators (NF-κB p65, TNF-α, NLRP3, IL-6) in serum and colon tissues. Furthermore, EA restored intestinal barrier integrity, as evidenced by improved mucosal ultrastructure and increased expression of tight junction proteins. Conclusion EA alleviates low-grade intestinal inflammation and visceral hypersensitivity in IBS-D rats. The therapeutic effect is mediated, at least in part through upregulation of lncRNA TUG1, which sponges miR-127-3p to inhibit the NF-κB p65 signaling pathway, thereby reducing inflammatory cytokine release and repairing the intestinal epithelial barrier. These findings suggest the TUG1/miR-127/NF-κB axis as a candidate therapeutic target for EA in IBS-D.

Electroacupuncture alleviates Parkinson's disease-related pain by inhibiting microglial NLRP3-ASC inflammasome in the amygdala

This study aimed to investigate the role of microglia and NOD-like receptor protein 3 (NLRP3) inflammasome-mediated neuroimmune pathways in the analgesic effects of electroacupuncture (EA) in a mouse model of Parkinson's disease (PD). Male C57BL/6 mice (8 weeks old) were randomly assigned to the control, PD model, and PD + EA groups. PD was induced by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), while control mice received saline. EA was administered to the motor cortex once daily for five consecutive days in the PD + EA group, whereas PD model mice were restrained without receiving EA stimulation. Behavioral assessments were performed to evaluate motor function and nociceptive sensitivity. Immunohistochemistry, immunofluorescence, and western blot analyses were used to quantify tyrosine hydroxylase (TH), ionized calcium-binding adapter molecule 1 (Iba-1), NLRP3 inflammasome components, and inflammatory cytokines in key brain regions. Compared with control mice, PD model mice showed reduced motor performance and heightened nociceptive sensitivity, accompanied by a decrease in TH-positive neurons and an increase in Iba-1-positive microglia in both the substantia nigra and amygdala. EA significantly improved motor performance and increased pain thresholds. Moreover, EA preserved TH-positive neurons, suppressed microglial activation, and downregulated the expression of NLRP3, ASC, caspase-1, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the amygdala. These findings suggest that EA alleviates PD-related pain, possibly by modulating microglial activation and NLRP3 inflammasome signaling in the amygdala, thereby reducing neuroinflammation.

Targeting TWEAK to enhance mitochondrial biogenesis and attenuate age-related muscle mass loss

Findings indicate that TWEAK suppression may represent a promising strategy for preserving muscle mass and metabolic homeostasis during aging, though its capacity to fully restore functional capacity requires further investigation.

Cryptotaenia japonica extract attenuates glucocorticoid-induced muscle atrophy via regulation of the AKT/mTOR–FOXO/E3 ubiquitin ligase axis

Sarcopenia, characterized by progressive loss of skeletal muscle mass and function, is exacerbated by chronic glucocorticoid exposure, which activates catabolic signaling pathways and accelerates muscle protein degradation. Although Cryptotaenia japonica Hassk (Apiaceae) has been reported to possess antioxidant and anti-inflammatory properties, its role in glucocorticoid-induced muscle atrophy remains unclear. In this study, we investigated the myoprotective effects of Cryptotaenia japonica extract (CJE) using both in vitro and in vivo models. C2C12 myotubes were treated with dexamethasone (Dex, 10 μM) in the presence or absence of CJE (10–100 μg/mL), and key signaling pathways were analyzed by Western blotting and confocal microscopy. In vivo, Dex-induced muscle atrophy was established in ICR mice, followed by oral administration of CJE (200 mg/kg/day). Muscle tissues were evaluated for protein expression, histological alterations, and serum GDF-8 levels. CJE treatment attenuated Dex-induced upregulation of the E3 ubiquitin ligases MuRF-1 and FBX32 and inhibited FOXO1 nuclear translocation in C2C12 myotubes. In dexamethasone-treated mice, CJE restored mTOR phosphorylation and normalized the dexamethasone-induced dysregulation of AKT phosphorylation, while suppressing the FOXO/E3 ubiquitin ligase catabolic axis. In Dex-treated mice, CJE reduced the expression of FOXO3a, MuRF-1, and FBX32, preserved muscle fiber architecture, and increased muscle fiber cross-sectional area. Furthermore, CJE modulated circulating GDF-8 levels associated with muscle atrophy. Collectively, these findings demonstrate that CJE mitigates glucocorticoid-induced muscle atrophy by coordinately regulating the AKT/mTOR–FOXO/E3 ubiquitin ligase signaling axis. These results suggest that CJE may serve as a promising natural therapeutic candidate for the prevention of sarcopenia and muscle-wasting conditions.