Electroacupuncture Facilitates the Regulation of Inflammation in the Conjunctiva of Rabbits With Dry Eye Syndrome via the α7nAChR-HMGB1 Signaling Pathway.

Abstract

​ Altered homeostasis of the ocular surface microenvironment is a hallmark of dry eye disease (DED). The alpha-7 nicotinic acetylcholine receptor (α7nAChR) plays a key role in DED pathophysiology. In this study, we established a rabbit model of DED using scopolamine hydrobromide (Scop) to determine the effect of electroacupuncture (EA) on ocular surface damage in DED and to explore its underlying mechanisms.​ Methods: New Zealand White rabbits (1.5-2.0 kg) were subcutaneously administered Scop for 21 days prior to EA treatment. After 35 days, the homeostasis of the ocular surface microenvironment was evaluated using the Schirmer I test (SIT), tear break-up time (BUT), corneal fluorescein (FL) staining, and measurement of tear osmolarity. The expression levels of ACh, α7nAChR, and high mobility group box 1 (HMGB1) were detected via histopathological examination of the cornea, lacrimal glands, and conjunctiva, combined with immunohistochemistry and western blotting. Additionally, protein chip technology was used to determine the expression levels of downstream factors.​ Results: EA stimulation significantly improved the homeostasis of the ocular surface microenvironment, as evidenced by increased SIT values and BUT, reduced corneal FL intensity, and decreased tear osmolarity. It also alleviated pathological damage to the cornea, conjunctiva, and lacrimal glands; upregulated the expression of ACh and α7nAChR; and downregulated the expression of HMGB1 and related inflammatory factors. However, these changes were reversed following administration of α-Bungarotoxin.​ Conclusion: EA stimulation improves ocular surface homeostasis and reduces inflammation in DED, potentially via activation of the α7nAChR signaling pathway, which in turn inhibits the expression of HMGB1 and inflammatory factors.​.