Farhangi Mahdieh Abbasalizad, Nameni Ghazaleh, Hajiluian Ghazaleh, Mesgari-Abbasi Mehran
Drug Applied Research Center, Nutrition Research Center, Department of Community Nutrition, Tabriz University of Medical Sciences, Attar Neyshabouri Street, Tabriz, Iran.
Student Research Committee, Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
BMC Cardiovasc Disord. 2017 Jun 19;17(1):161. doi: 10.1186/s12872-017-0597-z.
Obesity is associated with numerous metabolic and inflammatory disorders. The current study was aimed to evaluate the effects of vitamin D administration on the markers of oxidative stress and inflammation in the cardiac tissue of high-fat diet induced obese rats.
In the beginning of the study, 40 male Wistar rats were divided into two groups: normal diet (ND) and high fat diet (HFD) for 16 weeks; then each group subdivided into two groups including: ND, ND + vitamin D, HFD and HFD + vitamin D. Vitamin D supplementation was done for 5 weeks at 500 IU/kg dosage. Tumor necrosis factor (TNF)-α concentration and markers of oxidative stress including glutathione peroxidase (GPx), superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT) concentrations in the cardiac tissue and serum concentrations of lipids in rats were determined using ELISA kits and spectrophotometry methods respectively.
According to our results, GPx activity in ND and ND + vitamin D group was significantly higher compared with HFD group. Similarly, SOD activity was also significantly increased in ND + vitamin D group compared with ND and HFD groups. Moreover, vitamin D administration, significantly reduced catalase activity in ND + vitamin D and HFD + vitamin D groups (P < 0.05). TNF-α concentration in heart tissue in ND + vitamin D group significantly reduced compared with ND group. Cardiac tissue MDA concentration in baseline or after vitamin D administration did not changed significantly.
Vitamin D improved cardiac oxidative stress and inflammatory markers in HFD induced obese rats. Further studies in human models are needed to further confirm the use of this nutrient in daily clinical practice.
肥胖与多种代谢和炎症性疾病相关。本研究旨在评估给予维生素D对高脂饮食诱导的肥胖大鼠心脏组织氧化应激和炎症标志物的影响。
在研究开始时,将40只雄性Wistar大鼠分为两组:正常饮食(ND)组和高脂饮食(HFD)组,持续16周;然后每组再分为两组,包括:ND组、ND + 维生素D组、HFD组和HFD + 维生素D组。以500 IU/kg的剂量补充维生素D,持续5周。分别使用ELISA试剂盒和分光光度法测定大鼠心脏组织中肿瘤坏死因子(TNF)-α浓度以及氧化应激标志物,包括谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)、丙二醛(MDA)和过氧化氢酶(CAT)的浓度,以及大鼠血清脂质浓度。
根据我们的结果,ND组和ND + 维生素D组的GPx活性显著高于HFD组。同样,与ND组和HFD组相比,ND + 维生素D组的SOD活性也显著增加。此外,给予维生素D后,ND + 维生素D组和HFD + 维生素D组的过氧化氢酶活性显著降低(P < 0.05)。与ND组相比,ND + 维生素D组心脏组织中的TNF-α浓度显著降低。基线时或给予维生素D后,心脏组织MDA浓度无显著变化。
维生素D改善了高脂饮食诱导的肥胖大鼠的心脏氧化应激和炎症标志物。需要在人体模型中进行进一步研究,以进一步证实这种营养素在日常临床实践中的应用。