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Author Spotlight: Decoding Corneal Neovascularization with Alkali Burn Model for Future Therapeutic Strategies
Published on: June 30, 2023
Sinomenine enhances recovery from corneal alkali burns by attenuating macrophage M1 polarization through modulating
1Department of Ophthalmology, Xi'an No.5 Hospital, Xi'an, 710000, China.
Abstract:
Corneal alkali burns trigger the infiltration of inflammation-associated macrophages, which can potentially lead to vision impairment. Although Sinomenine (SIN) is recognized for its anti-inflammatory properties, its role on the polarization of macrophages and its effects on corneal alkali injury remain inadequately understood. In this study, corneal alkali damage was induced using NaOH. HE staining and immunohistochemistry were conducted to assess macrophage infiltration in corneal tissues. Macrophages were isolated via flow cytometry assay. Quantitative real-time PCR (qRT-PCR) was employed to examine the expression of genes associated with macrophage polarization. The results indicated an increase in macrophage infiltration and M1 polarization in mice subjected to corneal alkali injury. Sinomenine treatment effectively inhibited the polarization of M1 macrophages in the cornea. In mice treated with Sinomenine post-injury, there was a reduction in the expression of the m6A methylation writer protein METTL3 in macrophages, which led to an upregulation of IRAKM expression. The elevated IRAKM expression subsequently inhibited the TLR4 inflammatory pathway and reduced corneal inflammatory cell infiltration, ultimately ameliorating corneal alkali burns. Sinomenine attenuates M1 macrophage polarization through upregulating IRAKM by inhibiting the expression of the m6A methylation writer protein METTL3 in macrophages, leading to enhanced outcomes in corneal alkali injuries.
Insights
Sinomenine (SIN) effectively treats corneal alkali burns by inhibiting M1 macrophage polarization. It reduces inflammation via METTL3 inhibition and IRAKM upregulation, improving vision outcomes.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Corneal alkali burns cause inflammation-associated macrophage infiltration, potentially impairing vision.
- Sinomenine (SIN) has anti-inflammatory effects, but its impact on macrophage polarization in corneal injury is unclear.
Purpose of the Study:
- To investigate Sinomenine's effects on macrophage polarization and corneal alkali injury.
- To elucidate the molecular mechanisms underlying Sinomenine's therapeutic action.
Main Methods:
- Corneal alkali burns induced in mice using NaOH.
- Histopathology (HE staining) and immunohistochemistry for macrophage infiltration.
- Macrophage isolation (flow cytometry) and gene expression analysis (qRT-PCR).
Main Results:
- Corneal alkali injury increased macrophage infiltration and M1 polarization.
- Sinomenine treatment inhibited M1 macrophage polarization.
- Sinomenine reduced METTL3 expression, upregulated IRAKM, inhibited the TLR4 pathway, and decreased inflammatory cell infiltration.
Conclusions:
- Sinomenine ameliorates corneal alkali burns by attenuating M1 macrophage polarization.
- This occurs through inhibiting METTL3 and upregulating IRAKM, leading to reduced inflammation.

