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α-亚麻酸对庆大霉素诱导的小鼠耳毒性的保护作用。

Protective effect of alpha-linolenic acid on gentamicin-induced ototoxicity in mice.

作者信息

Kaplan Halil Mahir, Şingirik Ergin, Erdoğan Kıvılcım Eren, Doran Figen

机构信息

a Department of Pharmacology, Faculty of Medicine , Cukurova University , Adana , Turkey.

b Department of Pathology, Faculty of Medicine , Cukurova University , Adana , Turkey.

出版信息

Somatosens Mot Res. 2017 Sep;34(3):145-150. doi: 10.1080/08990220.2017.1356283. Epub 2017 Jul 31.

DOI:10.1080/08990220.2017.1356283
PMID:28760048
Abstract

Alpha-linolenic acid is one of the fatty acids known as omega 3. Previous studies have shown the antioxidant and anti-inflammatory effects of alpha-linolenic acid, which prevented cell damage by inhibiting apoptotic pathway. Also, it is known that gentamicin activates apoptotic mediators and causes necrosis in the kidney. Due to this reason, we planned a study to evaluate the protective effects of alpha-linolenic acid on gentamicin induced ototoxicity by evaluating inflammation and apoptotic mediators. For this purpose, 100 mg/kg gentamicin (i.p; intraperitoneally) and 200 mg/kg alpha-linolenic acid (gavage) are administered to mice for 9 days. On 9th and 10th days, rotarod performance was assessed to test the effect of gentamicin and alpha-linolenic acid treatment on the motor coordination of mice. Gentamicin treatment decreased fall latency of mice and gentamicin treatment together with alpha-linolenic acid increased fall latency of mice. Gentamicin treatment also increased expression of phospholipase A2(plA2), cyclooxygenase-2(COX-2) and inducible nitric oxide syntheses (iNOS). Furthermore, it increased Bax and caspase-3, which are proapoptotic proteins and decreased bcl-2 that is an antiapoptotic protein. Gentamicin treatment together alpha-linolenic acid recovered the change of expression of these enzymes. In conclusion, this study showed that alpha-linolenic acid will be useful to prevent gentamicin-induced ototoxicity by inhibiting apoptosis and inflammation.

摘要

α-亚麻酸是被称为ω-3的脂肪酸之一。先前的研究表明,α-亚麻酸具有抗氧化和抗炎作用,可通过抑制凋亡途径预防细胞损伤。此外,已知庆大霉素会激活凋亡介质并导致肾脏坏死。基于此,我们计划开展一项研究,通过评估炎症和凋亡介质来评价α-亚麻酸对庆大霉素诱导的耳毒性的保护作用。为此,给小鼠腹腔注射100mg/kg庆大霉素及灌胃200mg/kgα-亚麻酸,持续9天。在第9天和第10天,评估转棒试验表现以测试庆大霉素和α-亚麻酸治疗对小鼠运动协调性的影响。庆大霉素治疗缩短了小鼠的跌落潜伏期,而庆大霉素与α-亚麻酸联合治疗则延长了小鼠的跌落潜伏期。庆大霉素治疗还增加了磷脂酶A2(plA2)、环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达。此外,它增加了促凋亡蛋白Bax和半胱天冬酶-3,并降低了抗凋亡蛋白bcl-2。庆大霉素与α-亚麻酸联合治疗恢复了这些酶表达的变化。总之,本研究表明,α-亚麻酸通过抑制凋亡和炎症,对预防庆大霉素诱导的耳毒性有效。

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