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

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.

Curcumin mitigates neurotoxic and neurobehavioral changes of gentamicin and sodium salicylate in rats by adjusting oxidative stress and apoptosis.

Currently, antibiotics and salicylates are the most highly consumed medications worldwide. The side effects of these pharmaceuticals on the nervous system have been little investigated. Thus, this study aimed to examine the influence of the gentamicin (GM) and sodium salicylates (SS) on neurobehavioral functions, including locomotors function, memory, and sensorimotor functions together with gamma-aminobutyric acid (GABA) neurotransmitter levels. Also, oxidative stress, lipid peroxidation, and apoptotic indicators of brain tissue were assessed. Additionally, the histopathological architecture of brain tissues was investigated. This study also evaluated the curcumin (CUR) efficacy to counteract the GM or SS induced neurotoxic impacts in rats. For this purpose, seven groups were administered physiological saline (1 ml/rat; orally), olive oil (1 ml/rat; orally), CUR (50 mg/kg bwt; orally), GM (120 mg/kg bwt; intraperitoneally), SS (300 mg /kg bwt; intraperitoneally), CUR + GM, or CUR + SS for consecutive 15 days. The results revealed that GM and SS exposure evoked impaired memory, sensorimotor deficit functions, and depressive-like behavior together with the depletion of GABA. GM and SS exposure elevated malondialdehyde and Caspase-3 levels, but total antioxidant capacity and Bcl-2 levels were reduced. Besides, GM and SS exposure induced distinct pathological perturbations in cerebral cortices and hippocampus tissues. CUR significantly reversed the GM and SS harmful impacts. In conclusion, these findings verified that CUR could be a biologically efficient protective intervention against GM and SS induced neurotoxic impacts and neurobehavioral aberrations.