English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

This study evaluated the protective effects of naringin (NRG) against 5-fluorouracil (5-FU)-elicited neurotoxicity. The animals were orally administered with NRG and subsequently injected with 5-FU. Injection of 5-FU caused depression in cerebral antioxidant enzymes, including glutathione peroxidase, superoxide dismutase, catalase, reduced glutathione and total protein levels, whereas malondialdehyde and acetylcholinesterase levels/activities were considerably upregulated. In addition, 5-FU-triggered cerebral pro-inflammation was shown via significantly increased levels of pro-inflammatory cytokines, inducible nitric oxide synthase, nuclear factor-ĸB, and caspase-3. Furthermore, necrotic and inflammatory histopathological lesions were observed in the cerebral tissues. Interestingly, the NRG administration considerably inhibited 5-FU-instigated cerebral oxido-inflammatory and apoptotic parameters in the treated animals. Thus, NRG could mitigate the neurotoxicity of 5-FU via the inhibition of oxido-inflammation and apoptosis in rats. These results suggested that NRG may have a relevant therapeutic importance in the management of 5-FU-elicited neurotoxicity.

Naringin ameliorates 5-fluorouracil elicited neurotoxicity by curtailing oxidative stress and iNOS/NF-ĸB/caspase-3 pathway