Ferulic acid may work well in preventing and treating ionizing radiation-induced cataract.

Protective effects of ferulic acid against ionizing radiation-induced oxidative damage in rat lens through activating Nrf2 signal pathway.

Ying-Nien Chen, Jiao Shen, Xian H Zhang, Wei Gao, Qing Cao, Fangfang Yan, C Xue

Int J Ophthalmol

Jan 1, 2023

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Abstract

AIM: To examine the protection of ferulic acid (FA) against ionizing radiation (IR)-induced lens injury in rats, as well as the underlying mechanisms. METHODS: FA (50 mg/kg) was administered to rats for 4 consecutive days before they were given 10 Gyγ-radiation, as well as for 3 consecutive days afterward. Two weeks after radiation, the eye tissues were collected. Histological alterations were evaluated by hematoxylin-eosin staining. Enzyme linked immunosorbent assay (ELISA) was utilized to assess the activities of glutathione reductase (GR) and superoxide dismutase (SOD), as well as the levels of glutathione (GSH) and malondialdehyde (MDA) in the lenses. The protein and mRNA levels of Bcl-2, caspase-3, Bax, heme oxygenase-1 (HO-1), and glutamate-cysteine ligase catalytic subunit (GCLC) were quantified using Western blot and quantitative reverse transcription polymerase chain reaction, respectively. With nuclear extracts, the nuclear factor erythroid-2 related factor (Nrf2) protein expressions in the nuclei were also measured. RESULTS: Rats exposed to IR showed lens histological alterations which could be alleviated by FA. FA treatment reversed apoptosis-related markers in IR-induced lens, as evidenced by lower levels of Bax and caspase-3 and higher level of Bcl-2. Furthermore, IR induced oxidative damage manifested by decreased GSH level, increased MDA level, and decreased SOD and GR activities. FA boosted nuclear translocation of Nrf2 and increased the expressions of HO-1 and GCLC to inhibit oxidative stress, as evidenced by an increase in GSH, a decrease in MDA, and an increase in GR and SOD activities. CONCLUSION: FA may work well in preventing and treating IR-induced cataract through promoting the Nrf2 signal pathway to attenuate oxidative damage and cell apoptosis.