ArticleInternational ophthalmology2023
Inhibition of p38 ameliorates axonal loss with modulation of autophagy in TNF-induced optic nerve damage.
Article in International ophthalmology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Intravitreal injection of SARM1 siRNA in TNF-induced optic nerve degeneration.International ophthalmology · 2025Article
- Axonal protection by combination of ripasudil and brimonidine with upregulation of p-AMPK in TNF-induced optic nerve degeneration.International ophthalmology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeA relationship between p38 and autophagy remains debated. The aim of the current study is to investigate whether an inhibitor of p38 prevents axon loss induced by TNF and whether it affects autophagy.
methodsRats were given intravitreal injection of TNF, TNF plus SB203580, a p38 inhibitor, or SB203580 alone. Immunoblot analysis was performed to examine p62 expression which is a marker of autophagic flux and LC3-II expression which is an autophagy marker in optic nerves 1 week after intravitreal injection. Morphometric analysis of axons was performed to evaluate the effects of SB203580 against TNF-induced optic nerve damage 2 weeks after intravitreal injection. Immunohistochemical analysis was performed to evaluate the expressions of LC3, neurofilament, phosphorylated p38 and p62 in the optic nerve.
resultsQuantification of axon number showed that TNF-induced axon loss was significantly protected by SB203580. Immunoblot analysis showed that the increase of p62 induced by TNF was totally eliminated by SB203580, and the SB203580 alone injection decreased the expression of p62. The level of LC3-II was significantly upregulated in the TNF plus SB203580 group compared with the TNF alone group, and the SB203580 alone injection increased the expression of LC3-II. Immunohistochemical analysis showed that LC3 immunoreactivity was found in the neurofilament positive fibers and that these immunoreactivities were enhanced by SB203580. Some colocalizations of p-p38 and p62 were observed in the TNF-treated optic nerve.
conclusionThese results suggest that inhibition of p38 exerts axonal protection with upregulated autophagy in TNF-induced optic nerve damage.
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