Salari Mahdieh, Zare Mehrjerdi Fatemeh, Yadegari Maryam, Rezvani Mohammad Ebrahim, Shahrokhi Raeini Azadeh
International Campus, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Yazd Neuroendocrine Research Center, Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services, Yazd, Iran.
Naunyn Schmiedebergs Arch Pharmacol. 2023 Jun;396(6):1325-1336. doi: 10.1007/s00210-023-02405-9. Epub 2023 Feb 2.
Sulfur dioxide (SO) is a toxic gas with harmful effects on various organs. However, recent studies have confirmed the protective effect of SO on ischemic heart disease, atherosclerosis, and lung infections. Therefore, the present study was designed to investigate the effect of endogenous SO on depression. The chronic unpredictable mild stress (CUMS) model was performed to cause depression. Depression-like behaviors in animals were determined using an open-field test, forced swimming test, and sucrose consumption. Animal spatial learning and memory were also assessed using the Morris water maze. Besides, the oxidative status of the hippocampus and serum corticosterone level were evaluated. A reduction in the tendency to consume sucrose, mobility, and curiosity, as well as learning and memory disorders were observed in CUMS animals. Depressed animals treated with SO revealed a significant improvement in behavioral and cognitive functions. SO also reduced neuronal damage and lipid peroxidation of the hippocampus and serum corticosterone level in the CUMS group. Various shreds of evidence support a mutual relationship between inflammation and depression; also, growing studies show the role of oxidative stress in the pathogenesis of mood-related disorders such as depression. This study indicated that increased hippocampal malondialdehyde (MDA) and serum corticosterone levels can be due to the existence of oxidative stress and possible activation of inflammatory processes. SO donors diminished MDA and corticosterone levels in depressed animals. According to the study results, SO may be able to reduce tissue damage and eventually behavioral disorders caused by depression by lowering oxidative stress and inflammation.
二氧化硫(SO)是一种对多种器官有有害影响的有毒气体。然而,最近的研究证实了SO对缺血性心脏病、动脉粥样硬化和肺部感染具有保护作用。因此,本研究旨在探讨内源性SO对抑郁症的影响。采用慢性不可预测轻度应激(CUMS)模型诱导抑郁症。通过旷场试验、强迫游泳试验和蔗糖消耗试验来测定动物的抑郁样行为。还使用莫里斯水迷宫评估动物的空间学习和记忆能力。此外,评估海马体的氧化状态和血清皮质酮水平。在CUMS动物中观察到蔗糖消耗倾向、活动能力和好奇心降低,以及学习和记忆障碍。用SO治疗的抑郁动物在行为和认知功能方面有显著改善。SO还减少了CUMS组中海马体的神经元损伤和脂质过氧化以及血清皮质酮水平。各种证据支持炎症与抑郁症之间存在相互关系;此外,越来越多的研究表明氧化应激在抑郁症等情绪相关疾病的发病机制中起作用。本研究表明,海马体丙二醛(MDA)和血清皮质酮水平升高可能是由于氧化应激的存在以及炎症过程可能被激活。SO供体降低了抑郁动物的MDA和皮质酮水平。根据研究结果,SO可能能够通过降低氧化应激和炎症来减少组织损伤,并最终减轻由抑郁症引起的行为障碍。