Abstract
Myopia is a common ocular disorder characterized by excessive axial elongation, and effective strategies for limiting its progression remain limited. This study investigated whether acupuncture attenuates myopia progression in a guinea pig model of form-deprivation myopia and examined the involvement of scleral inflammation and brain-derived neurotrophic factor (BDNF)-mediated neurotrophic signaling. Guinea pigs were randomly assigned to control, myopia, acupuncture-only, and myopia plus acupuncture groups for phenotypic evaluation. Additional sham acupuncture and myopia-plus-acupuncture groups, combined with subconjunctival cyclotraxin B (CTX-B) administration, were included to evaluate acupuncture specificity and the involvement of BDNF/tropomyosin receptor kinase B (TrkB) signaling. Following intervention, refractive error and axial length were measured in the primary treatment groups. Scleral remodeling markers, including collagen type I alpha 1 (COL1A1) and α-smooth muscle actin (α-SMA); inflammatory mediators, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and nuclear factor kappa B (NF-κB); and neurotrophic factors, including BDNF, TrkB, nerve growth factor, and neurotrophin-4, were evaluated using enzyme-linked immunosorbent assay, quantitative reverse transcription PCR, Western blotting, and immunofluorescence. Acupuncture was associated with reduced myopic refractive shifts and axial elongation. At the final observation time point, axial elongation was lower in the myopia plus acupuncture group than in the myopia group (ΔAL, 0.77 ± 0.19 mm vs. 1.42 ± 0.20 mm; Cohen's d = 1.51). Acupuncture also reduced scleral IL-1β, IL-6, and NF-κB expression and increased BDNF, TrkB, nerve growth factor, and neurotrophin-4 expression. Sham acupuncture showed limited effects on these molecular changes, whereas CTX-B attenuated acupuncture-associated alterations in BDNF/TrkB signaling, extracellular matrix remodeling, and inflammatory markers. These findings suggest that acupuncture attenuates myopia progression through coordinated regulation of scleral inflammation and neurotrophic support involving BDNF/TrkB signaling.