Azithromycin and Gallic acid alleviate neurobehavioral deficits in rats resulting from chronic Aflatoxin B1 exposure

IF 2.4 4区 医学 Q2 PHARMACOLOGY & PHARMACY
Solomon Owumi , Joseph Chimezie , Idris O. Bello , Moses T. Otunla , Uche Arunsi , Ayomide P. Akomolafe , Jesutosin O. Babalola , Chioma E. Irozuru , Olatunde O. Owoeye
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引用次数: 0

Abstract

Aflatoxin B1 (AFB1) is a mycotoxin known for its liver toxicity and cancer risk, as well as neurotoxic effects causing motor and cognitive issues in humans and animals. Ongoing research into protecting against AFB1 damage has recently focused on antioxidant and anti-inflammatory agents. Gallic acid (GA), a low molecular weight triphenolic acid, demonstrates notable anti-oxidative and anti-inflammatory activities. Furthermore, Azithromycin (AZT), an antibiotic, has shown promise in mitigating inflammatory stress in experimental models. GA and AZT may help protect against AFB1-induced neurobehavioral deficits in rats. This experiment involved thirty-five rats randomly assigned to seven cohorts (n = 5), over a 28-day treatment period. The study consisted of a control group given corn oil, a group exposed only to AFB1, and groups that received GA, AZT, or combinations of these substances with AFB1. The neurobehavioral status of the experimental rats was assessed using the Open Field Test (OFT) and Novel Object Recognition Test (NORT) on days 26 and 27, respectively. On day 28 following treatment, the Elevated Plus Maze (EPM), Y-maze, and Forced Swim Test (FST) were conducted. After behavioural evaluation, the rats were euthanised. The hippocampus and prefrontal cortex were dissected for biochemical analysis. Antioxidant enzyme activities (SOD, CAT, GPx, GST), GSH and TSH levels, acetylcholinesterase, and markers of oxidative stress (RONS, LPO) and inflammation (NO, MPO) were measured. AFB1 exposure raised oxidative stress markers, MPO, and AChE activity, while lowering antioxidant enzymes in the hippocampus and prefrontal cortex, indicating notable neurotoxicity and signalling disruptions. Combined GA and AZT treatment improved antioxidant defence, reduced inflammation, and restored AChE activity. Neurobehavioral tests indicated better motor and cognitive function after AFB1 exposure. These results suggest that GA and AZT together offer strong protection against AFB1-induced neurotoxicity via their antioxidant and anti-inflammatory effects.

Abstract Image

阿奇霉素和没食子酸减轻慢性黄曲霉毒素B1暴露引起的大鼠神经行为缺陷
黄曲霉毒素B1 (AFB1)是一种真菌毒素,以其肝毒性和癌症风险以及导致人类和动物运动和认知问题的神经毒性作用而闻名。目前正在进行的防止AFB1损伤的研究主要集中在抗氧化剂和抗炎剂上。没食子酸(GA)是一种低分子量的三酚酸,具有显著的抗氧化和抗炎活性。此外,阿奇霉素(AZT),一种抗生素,在实验模型中显示出减轻炎症应激的希望。GA和AZT可能有助于预防afb1诱导的大鼠神经行为缺陷。本实验涉及35只大鼠,随机分为7个队列(n = 5),治疗期28天。该研究包括给予玉米油的对照组,仅暴露于AFB1的组,以及接受GA, AZT或这些物质与AFB1的组合的组。第26天和第27天分别采用开放场测试(Open Field Test, OFT)和新目标识别测试(Novel Object Recognition Test, NORT)评估实验大鼠的神经行为状态。治疗后第28天进行高架+迷宫(EPM)、y型迷宫(Y-maze)和强迫游泳测试(FST)。行为评估后,对大鼠实施安乐死。解剖海马和前额叶皮层进行生化分析。测定抗氧化酶活性(SOD、CAT、GPx、GST)、GSH和TSH水平、乙酰胆碱酯酶、氧化应激标志物(RONS、LPO)和炎症标志物(NO、MPO)。AFB1暴露增加了氧化应激标志物、MPO和AChE活性,同时降低了海马和前额皮质的抗氧化酶,表明显著的神经毒性和信号中断。GA和AZT联合治疗可改善抗氧化防御,减少炎症,恢复乙酰胆碱酯酶活性。神经行为测试显示AFB1暴露后运动和认知功能更好。这些结果表明,GA和AZT通过其抗氧化和抗炎作用,对afb1诱导的神经毒性具有很强的保护作用。
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来源期刊
Toxicon
Toxicon 医学-毒理学
CiteScore
4.80
自引率
10.70%
发文量
358
审稿时长
68 days
期刊介绍: Toxicon has an open access mirror Toxicon: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. An introductory offer Toxicon: X - full waiver of the Open Access fee. Toxicon''s "aims and scope" are to publish: -articles containing the results of original research on problems related to toxins derived from animals, plants and microorganisms -papers on novel findings related to the chemical, pharmacological, toxicological, and immunological properties of natural toxins -molecular biological studies of toxins and other genes from poisonous and venomous organisms that advance understanding of the role or function of toxins -clinical observations on poisoning and envenoming where a new therapeutic principle has been proposed or a decidedly superior clinical result has been obtained. -material on the use of toxins as tools in studying biological processes and material on subjects related to venom and antivenom problems. -articles on the translational application of toxins, for example as drugs and insecticides -epidemiological studies on envenoming or poisoning, so long as they highlight a previously unrecognised medical problem or provide insight into the prevention or medical treatment of envenoming or poisoning. Retrospective surveys of hospital records, especially those lacking species identification, will not be considered for publication. Properly designed prospective community-based surveys are strongly encouraged. -articles describing well-known activities of venoms, such as antibacterial, anticancer, and analgesic activities of arachnid venoms, without any attempt to define the mechanism of action or purify the active component, will not be considered for publication in Toxicon. -review articles on problems related to toxinology. To encourage the exchange of ideas, sections of the journal may be devoted to Short Communications, Letters to the Editor and activities of the affiliated societies.
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