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Journal Article

Curcumin attenuates gentamicin and sodium salicylate ototoxic effects by modulating the nuclear factor-kappaB and apoptotic pathways in rats

Yasmina M. Abd-Elhakim; Sabry M. Abdel-Motal; Seham M. Malhat; Hend I. Mostafa; Walied M. Ibrahim; Rasha R. Beheiry; Attia A.A. Moselhy; Enas N. Said
Environmental Science and Pollution Research · Vol. 29, Issue 60 · pp. 89954-89968 · 2022

Abstract

This study aimed to investigate the effectiveness of curcumin (CCM) against gentamicin (GEN) and sodium salicylates (NaS)-induced ototoxic effects in rats. For 15 consecutive days, seven rat groups were given 1 mL/rat physiological saline orally, 1 mL/rat olive oil orally, 50 mg/kg bwt CCM orally, 120 mg/kg bwt GEN intraperitoneally, 300 mg/kg bwt NaS intraperitoneally, CCM+GEN, or CCM+NaS. The distortion product otoacoustic emission measurements were conducted. The rats’ hearing function and balance have been behaviorally assessed using auditory startle response, Preyer reflex, and beam balance scale tests. The serum lipid peroxidation and oxidative stress biomarkers have been measured. Immunohistochemical investigations of the apoptotic marker caspase-3 and the inflammatory indicator nuclear factor kappa (NF-κB) in cochlear tissues were conducted. GEN and NaS exposure resulted in deficit hearing and impaired ability to retain balance. GEN and NaS exposure significantly decreased the reduced glutathione level and catalase activity but increased malondialdehyde content. GEN and NaS exposure evoked pathological alterations in cochlear and vestibular tissues and increased caspase-3 and NF-κB immunoexpression. CCM significantly counteracted the GEN and NaS injurious effects. These outcomes concluded that CCM could be a naturally efficient therapeutic agent against GEN and NaS-associated ototoxic side effects. Graphical abstract

Bibliographic Information

JournalEnvironmental Science and Pollution Research
PublisherSpringer
Publication Date2022-12-01
Publication Year2022
Volume29
Issue60
Pages89954-89968
Document TypeJournal Article
eISSN1614-7499
DOI10.1007/s11356-022-21932-1

Access Information

NARA Access Coverage1994-01-01~Current
Journal Homepagehttps://www.springer.com/journal/11356
Publisher PageOpen Publisher Page
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