Abstract
Objective: The following study aimed to investigate the efficacy of curcumin at preventing amikacin neurotoxicity
 Methods: Twenty-four male Wister albino rats were randomly divided into four groups including-G (1): control group includes six rats, they were administered 0.5 ml of saline orally for 14 consecutive days. G (2): includes six rats; they were administered 200 mg/kg curcumin orally for 14 consecutive days. G (3): includes six rats, they were administered 300 mg/kg body weight/day of amikacin intraperitoneally for 14 consecutive days G (4): includes six rats, they were administered 200 mg/kg curcumin orally concurrently with 300 mg/kg body weight/day of amikacin. All animals were kept in the same conditions from feed, heat and humidity.
 Results: According to the result obtained after sacrification of all animals after the end of 14 d, Results revealed that amikacin at the dose rate of 300 mg/kg b. wt for 14 d induces significant changes in oxidative stress markers compared to the control group, a significant reduction in CAT. SOD. GSH (1.51±0.16, 77.00±0.73 and 84.06±4.42) respectively compared to control (3.63±0.11, 98.48±0.18 and 117.05±0.52) along with a significant increase in MDA activity (219.02±3.34) compared to control group (180.42±0.19), That indicate oxidative stress effect of it. On the beneficial side rats received amikacin 300 mg/kg B. wt I/p concurrently with 200 mg/kg b. wt curcumin for successive 14day result in a significant increase in CAT. SOD. GSH (2.23±0.09,92.00±0.26, 102.25±1.71) and decrease in MDA concentration (139.23±3.89) compared to amikacin treated group levels along with histopathological changes appear in brain tissue in the group treated with amikacin include nuclear pyknosis and degeneration in some neurons in the hippocampus, multiple focal eosinophilic plaque formation in the striatum also this results enhanced by activated caspase-3 expression in the brain tissue following amikacin administration.
 Conclusion: The present study proved that Oral administration of curcumin at the dose of 200 mg/kg for 14 d concurrently with amikacin significantly mitigates its neurotoxic and oxidative stress effects.
Highlights
IntroductionAmikacin is a broad-spectrum aminoglycoside antibiotic derived from kanamycin and is highly effective against gram-negative organisms (including gentamycin-resistant strains) as well as a few gram-positive organisms [1]
Amikacin is a broad-spectrum aminoglycoside antibiotic derived from kanamycin and is highly effective against gram-negative organisms as well as a few gram-positive organisms [1]
One of them is Curcumin is one of the most important medicinal plants. it is a herbaceous plant belonging to the ginger family, it extracts from the rhizomes of plant of curcuma longa [4], it exhibits a variety of therapeutic properties, including antioxidant [5], antiapoptotic activities [6, 7]
Summary
Amikacin is a broad-spectrum aminoglycoside antibiotic derived from kanamycin and is highly effective against gram-negative organisms (including gentamycin-resistant strains) as well as a few gram-positive organisms [1]. It binds mainly to 30s ribosomes and interferes with the initiation of protein synthesis, block the translation of mRNA and prematurely terminate the protein synthesis Like other aminoglycosides, it may cause nephrotoxicity, hepatotoxicity, ototoxicity, and neuromuscular block [2, 3]. It is a herbaceous plant belonging to the ginger family, it extracts from the rhizomes of plant of curcuma longa [4], it exhibits a variety of therapeutic properties, including antioxidant [5], antiapoptotic activities [6, 7]. It has a strong potency in inhibiting the generation of reactive oxygens species (ROS). Curcumin can cross the blood-brain barrier suggesting a possible cause of neuroprotective effect [8]
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