Adelani I B, Ogadi E O, Onuzulu C, Rotimi O A, Maduagwu E N, Rotimi S O
Department of Biochemistry, College of Science and Technology, Covenant University, Ota, Ogun State, Nigeria.
Department of Biochemistry, Chrisland University, Abeokuta, Ogun State, Nigeria.
Heliyon. 2020 Sep 14;6(9):e04842. doi: 10.1016/j.heliyon.2020.e04842. eCollection 2020 Sep.
The generation of reactive oxygen species (ROS) plays an essential role in the pathogenesis of several diseases. Its implication in inflammation has suggested a possible link between oxidative stress and activation/release of cytokines in precancerous states. Recent observational studies have suggested an association between inflammation and vitamin D deficiency; hence, suggesting that vitamin D could play a role in the pathogenesis of diseases. This study examined the antioxidant and anti-inflammatory potentials of vitamin D in diethylnitrosamine (DEN)-induced oxidative stress and inflammation in rats. Rats were divided into four experimental groups. While groups one and two were administered twice weekly with 30 mg/kg body weight DEN for six weeks, groups three and four were given normal saline. Groups one and three were fed with vitamin D deficient diet, while groups two and four were fed vitamin D diet during the experiment. After that, biomarkers of oxidative stress status were assayed spectrophotometrically. The concentration of inflammatory cytokines was determined using enzyme-linked immunosorbent assay (ELISA). DEN-induced vitamin D deficient diet group had increased antioxidant enzymes' activities. Also, there were elevated concentrations of thiobarbituric acid reactive substances (TBARS) and inflammatory cytokines in the same group. Vitamin D diet, however, reduced oxidative stress effects through the reduction in the activities of TBARS and caused a significant () increase in nitric oxide concentration. Vitamin D diet significantly () reduced the level of interleukin 1β and TNF-α produced in the deficiency state. These findings show that vitamin D may play an essential role in the regulation of hepatic oxidative stress and inflammatory responses.
活性氧（ROS）的产生在多种疾病的发病机制中起着至关重要的作用。其在炎症中的作用提示了氧化应激与癌前状态下细胞因子的激活/释放之间可能存在联系。最近的观察性研究表明炎症与维生素D缺乏之间存在关联；因此，提示维生素D可能在疾病的发病机制中发挥作用。本研究检测了维生素D对二乙基亚硝胺（DEN）诱导的大鼠氧化应激和炎症的抗氧化及抗炎潜力。将大鼠分为四个实验组。第一组和第二组每周两次给予30 mg/kg体重的DEN，持续六周，第三组和第四组给予生理盐水。第一组和第三组喂食维生素D缺乏饮食，而第二组和第四组在实验期间喂食维生素D饮食。之后，采用分光光度法检测氧化应激状态的生物标志物。使用酶联免疫吸附测定（ELISA）法测定炎性细胞因子的浓度。DEN诱导的维生素D缺乏饮食组抗氧化酶活性增加。此外，同一组中硫代巴比妥酸反应性物质（TBARS）和炎性细胞因子的浓度也升高。然而，维生素D饮食通过降低TBARS的活性减轻了氧化应激作用，并使一氧化氮浓度显著（）升高。维生素D饮食显著（）降低了缺乏状态下产生的白细胞介素1β和肿瘤坏死因子-α的水平。这些发现表明维生素D可能在肝脏氧化应激和炎症反应的调节中起重要作用。
