Abstract

Acetaminophen (APAP) is a well-known antipyretic and analgesic medicine. It is safe at therapeutic suggested level while overdose initiates oxidative stress and inflammation mediated neurochemical alteration in the brain. The aim of this study was to investigate the role of cinnamon oil (CO), which possesses potent antioxidant and anti-inflammatory activities against an overdose of APAP that induced oxidative stress and inflammation in male albino rats. APAP treated rats showed significant elevation of thiobarbituric acid-reactive substances (TBARS) and decreased level of GSH in brain tissue, which is recognized as a biomarker of oxidative stress. Antioxidant enzymes GPx, GR, SOD, and CAT activity was depleted in APAP group along with neurotoxicity biomarkers such as Na⁺-K⁺-ATPase and increased activity of acetylcholinesterase (AchE), monoamine oxidase (MAO), and upregulated pro-inflammatory cytokine was observed. CO significantly protected the diminished activity of the antioxidant enzyme and suppressed the upregulated cytokines in brain tissue. CO also attenuated the activity of neurotoxicity biomarker enzyme, decreased TBARS content, and an increased level of GSH. The present findings perceptibly confirmed that the nutraceutical property of CO ameliorates APAP induced oxidative stress and inflammation. Therefore, our findings suggested that CO could be an alternative nutraceutical substitute in APAP overdose poisoning.

摘要

对乙酰氨基酚 (APAP) 是一种众所周知的解热镇痛药。它在治疗建议的水平上是安全的，而过量服用会引发氧化应激和炎症介导的大脑神经化学变化。本研究的目的是研究肉桂油 (CO) 的作用，它具有有效的抗氧化和抗炎活性，可以对抗过量的 APAP，从而在雄性白化病大鼠中引起氧化应激和炎症。APAP 治疗的大鼠表现出硫代巴比妥酸反应物质 (TBARS) 显着升高和脑组织中 GSH 水平降低，这被认为是氧化应激的生物标志物。APAP 组的抗氧化酶 GPx、GR、SOD 和 CAT 活性以及神经毒性生物标志物如 Na ⁺ -K ^+被耗尽观察到 -ATP 酶和乙酰胆碱酯酶 (AchE)、单胺氧化酶 (MAO) 和上调的促炎细胞因子的活性增加。CO 显着保护了降低的抗氧化酶活性并抑制了脑组织中上调的细胞因子。CO 还减弱了神经毒性生物标志物酶的活性，降低了 TBARS 含量，并增加了 GSH 水平。目前的研究结果明显地证实了 CO 的营养特性改善了 APAP 诱导的氧化应激和炎症。因此，我们的研究结果表明，CO 可能是 APAP 过量中毒的替代营养品替代品。