<p>Introduction: Corneal injuries can lead to permanent damage that disrupts the integrity of the cornea and impairs vision. Photobiomodulation (PBM) is a non-invasive therapy that uses specific wavelengths of light to stimulate biological processes, leading to a range of therapeutic benefits. In this study, the effect of PBM on the alkali burn model was investigated, with a focus on its potential to promote cell proliferation and migration and reduce inflammation using 830&#xa0;nm of light. A wavelength of 830 nm was used for PBM treatment. After Alkali burn induction, rats were treated with 830 nm light every 12 h and the healing area was observed. Immunofluorescent staining of Ki67 demonstrated the proliferation of corneal epithelial cells. Clinical examination of corneal neovascularization and the opacity was assessed using a slit lamp. Immunohistochemistry was performed to compare the expression of inflammatory cytokines. Western blot analysis revealed a difference in the level of Rho-GTPase between the control and PBM group. PBM treatment promoted wound closure after alkali burn induction. The number of Ki67 positive cells increased in the PBM group than in the control. New blood vessel growth expanded from the limbal to the cornea after a week following the alkali burn in both groups, and no significant difference was observed in neovascularization score. However, corneal opacity was significantly reduced in the PBM group compared with the control group at 1 week (p = 0.029). Furthermore, immunohistochemistry revealed significantly reduced expression of IL-1β, IL-6, and TNF-α in the PBM group compared with the alkali burn control at 48 h, and corresponding mRNA expression levels of all three cytokines were also significantly decreased at both 48 h and 1 week. The expression of selected Rho-GTPase proteins (RhoA, RhoC) was increased in whole corneal tissue of the PBM group during the early healing phase. 830-nm PBM accelerated early corneal re-epithelialization by enhancing corneal epithelial cell migration and proliferation in vitro and in vivo. This recovery was accompanied by increased expression of selected Rho-GTPases (RhoA/RhoC), suggesting a potential involvement of cytoskeletal signaling in epithelial repair. Crucially, PBM established a robust anti-inflammatory environment by significantly downregulating key pro-inflammatory cytokines at both the transcriptional and translational levels, which successfully translated into a significant alleviation of subacute corneal opacity. Together, these findings support 830-nm PBM as a highly effective, non-invasive supportive strategy that facilitates therapeutic recovery after chemical corneal injury.</p><p>Clinical Trial Number: Not Applicable.</p>

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Promotive effects of 830-nm Photobiomodulation on corneal epithelial wound healing and rho-gtpase expression in a rat alkali burn model

  • Esther Jang,
  • Hoon Kim,
  • Kyongjin Cho

摘要

Introduction: Corneal injuries can lead to permanent damage that disrupts the integrity of the cornea and impairs vision. Photobiomodulation (PBM) is a non-invasive therapy that uses specific wavelengths of light to stimulate biological processes, leading to a range of therapeutic benefits. In this study, the effect of PBM on the alkali burn model was investigated, with a focus on its potential to promote cell proliferation and migration and reduce inflammation using 830 nm of light. A wavelength of 830 nm was used for PBM treatment. After Alkali burn induction, rats were treated with 830 nm light every 12 h and the healing area was observed. Immunofluorescent staining of Ki67 demonstrated the proliferation of corneal epithelial cells. Clinical examination of corneal neovascularization and the opacity was assessed using a slit lamp. Immunohistochemistry was performed to compare the expression of inflammatory cytokines. Western blot analysis revealed a difference in the level of Rho-GTPase between the control and PBM group. PBM treatment promoted wound closure after alkali burn induction. The number of Ki67 positive cells increased in the PBM group than in the control. New blood vessel growth expanded from the limbal to the cornea after a week following the alkali burn in both groups, and no significant difference was observed in neovascularization score. However, corneal opacity was significantly reduced in the PBM group compared with the control group at 1 week (p = 0.029). Furthermore, immunohistochemistry revealed significantly reduced expression of IL-1β, IL-6, and TNF-α in the PBM group compared with the alkali burn control at 48 h, and corresponding mRNA expression levels of all three cytokines were also significantly decreased at both 48 h and 1 week. The expression of selected Rho-GTPase proteins (RhoA, RhoC) was increased in whole corneal tissue of the PBM group during the early healing phase. 830-nm PBM accelerated early corneal re-epithelialization by enhancing corneal epithelial cell migration and proliferation in vitro and in vivo. This recovery was accompanied by increased expression of selected Rho-GTPases (RhoA/RhoC), suggesting a potential involvement of cytoskeletal signaling in epithelial repair. Crucially, PBM established a robust anti-inflammatory environment by significantly downregulating key pro-inflammatory cytokines at both the transcriptional and translational levels, which successfully translated into a significant alleviation of subacute corneal opacity. Together, these findings support 830-nm PBM as a highly effective, non-invasive supportive strategy that facilitates therapeutic recovery after chemical corneal injury.

Clinical Trial Number: Not Applicable.