Retinal detachment is a serious ocular disease leading to photoreceptor degeneration and vision loss. However, the mechanism of photoreceptor degeneration remains unclear. The aim of this study was to investigate the altered metabolism pathway and physiological changes after
retinal detachment. Eight-week-old male SD rats were fed, and the model of
retinal detachment was established by injecting
hyaluronic acid into the
retinal space. The rats were euthanized 3 days after RD, and the
retinal tissues were sectioned for analysis. Untargeted
lipid chromatography-mass spectrometry lipidomic was performed to analyze the metabolite changes. A total of 90 significant metabolites (34 in anionic and 56 in cationic models) were detected after
retinal detachment. The main pathways were (1)
histidine metabolism; (2)
phenylalanine,
tyrosine, and
tryptophan biosynthesis; and (3)
glycine,
serine, and
threonine metabolism. The key genes corresponding to each metabolic pathway were verified from the Gene Expression Omnibus (GEO) database of human
retinal samples. The results indicated that the production of
histamine by
histidine decarboxylase from
histidine reduced after RD (p < 0.05).
Xanthine,
hypoxanthine,
guanine, and
guanosine decreased after RD (p < 0.05). Decreased
xanthine and
hypoxanthine may reduce the
antioxidant ability. The decreased
guanosine could not provide enough sources for
inosine monophosphate production.
Tyrosine is an important
neurotransmitter and was significantly reduced after RD (p < 0.05).
Citrate was significantly reduced with the increase of
ATP-citrate lyase enzyme (ACLY) (p < 0.05). We inferred that
lipid oxidation might increase rather than
lipid biogenesis. Thus, this study highlighted the main changes of metabolite and physiological process after RD. The results may provide important information for photoreceptor degeneration.