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替莫喹酮可改善氨基糖苷类抗生素(如阿米卡星)诱导的大鼠脑组织氧化损伤。

Thymoquinone ameliorates amikacin induced oxidative damage in rat brain tissue.

机构信息

Department of Medical Biochemistry, Vocational School of Health Services, University of Adıyaman, Adıyaman, Turkey.

Department of Histology, and Embryology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.

出版信息

Biotech Histochem. 2023 Jan;98(1):38-45. doi: 10.1080/10520295.2022.2087905. Epub 2022 Jul 11.

DOI:10.1080/10520295.2022.2087905
PMID:35811486
Abstract

We investigated the potential neuroprotective effects of thymoquinone (TQ) on amikacin (AK) induced oxidative damage in rat brain. We used 21 male rats divided randomly into three equal groups. The control group was injected intraperitoneally (i.p.) with 0.5 ml 0.9% aqueous NaCl and given 1 ml 0.9% aqueous NaCl orally. The AK group was administered 1.2 g/kg aqueous AK i.p. as a single dose on the day 3 of the study. The AK + TQ group was given a single 1.2 g/kg dose of AK i.p. on the day 3 of the study plus 40 mg/kg/day TQ by oral gavage daily. Treatment with TQ increased serum ferritin and decreased serum calcium levels significantly. TQ also decreased NADPH oxidase-2, NADPH oxidase-4, and caspase-3 levels. Decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) and catalase (CAT) activities were detected in the AK + TQ group compared to the AK group. TQ administration inhibited lipid peroxide formation and blocked oxidative reactions, which reduced the MDA level and increased SOD and CAT activities induced by AK. Oxidative damage caused by AK was ameliorated by TQ treatment owing to its antioxidative and anti-apoptotic effects. TQ may be a potential therapeutic agent for reducing the severity of AK induced oxidative damage to the brain.

摘要

我们研究了百里醌(TQ)对氨基糖苷类抗生素(AK)诱导的大鼠脑内氧化损伤的潜在神经保护作用。我们使用了 21 只雄性大鼠,随机分为三组。对照组经腹腔注射(i.p.)0.5ml 0.9%生理盐水,并口服 1ml 0.9%生理盐水。AK 组在研究的第 3 天给予 1.2g/kg 的 AK 水溶液 i.p.作为单次剂量。AK+TQ 组在研究的第 3 天给予 1.2g/kg 的 AK i.p.单次剂量,同时每天口服给予 40mg/kg 的 TQ。TQ 治疗可显著增加血清铁蛋白水平,降低血清钙水平。TQ 还降低了 NADPH 氧化酶-2、NADPH 氧化酶-4 和半胱氨酸天冬氨酸蛋白酶-3 的水平。与 AK 组相比,AK+TQ 组的丙二醛(MDA)水平降低,超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性增加。TQ 可抑制脂质过氧化物的形成并阻断氧化反应,从而降低 AK 诱导的 MDA 水平,并增加 SOD 和 CAT 活性。TQ 治疗可减轻 AK 引起的氧化损伤,这归因于其抗氧化和抗凋亡作用。TQ 可能是一种潜在的治疗药物,可减轻 AK 对大脑引起的氧化损伤的严重程度。

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