Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran.
Department of Biochemistry, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Mol Biol Rep. 2021 Dec;48(12):7865-7873. doi: 10.1007/s11033-021-06810-2. Epub 2021 Oct 12.
Chronic stress increases the production of pro-inflammatory cytokines and oxidative stress in the brain, which underlay cognitive and psychological problems. In addition to the anti-depressants, vitamin D is known to act as an anti-inflammatory and anti-oxidative agent. This study investigates the specific effects of vitamin D in protecting hippocampus and pre-frontal cortex (PFC) against chronic mild stress (CMS)-induced activation of pro-inflammatory cytokines IL-6 and TNF-α and decreasing the activation of anti-oxidative enzymes super oxide dismutase (SOD) and glutathione peroxidase (GPx).
Rats were exposed to CMS for 3 weeks. Two groups of rats received vitamin D (5 and 10 μg/kg) and another received fluoxetine (5 mg/kg) along with CMS. Control groups were not exposed to CMS, but received treatments similar to CMS groups. Serum corticosterone and IL-6, TNF-α and SOD and GPx levels in the hippocampus and PFC were measured at the end of three weeks. CMS significantly increased corticosterone, IL-6, TNF-α and decreased SOD and GPx levels (P < 0.0001) in hippocampus and PFC. Vitamin D treatment reduced corticosterone levels (P < 0.01), increased SOD (P < 0.0001) and GPx (P < 0.01) and decreased IL-6 and TNF-α (P < 0.0001) levels in the hippocampus and PFC compared to rats treated with vitamin D vehicle. Vitamin D-10 regulation of SOD and IL-6 levels was more effective than fluoxetine (P < 0.0001 and P < 0.01, respectively, in hippocampus).
This study suggests that vitamin D effectively protects the key regions of the brain related to cognition and affective behavior, against the inflammation and oxidative stress caused by the chronic stress.
慢性应激会增加大脑中促炎细胞因子和氧化应激的产生，从而导致认知和心理问题。除了抗抑郁药，维生素 D 也被认为具有抗炎和抗氧化作用。本研究旨在探讨维生素 D 对慢性轻度应激（CMS）诱导的促炎细胞因子白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α）激活的保护作用，以及对超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）等抗氧化酶的激活作用。
大鼠接受 CMS 处理 3 周。两组大鼠分别接受 5 和 10μg/kg 的维生素 D 治疗，另一组大鼠接受氟西汀（5mg/kg）和 CMS 联合治疗。对照组大鼠不接受 CMS 处理，但接受与 CMS 组类似的治疗。在 CMS 处理 3 周后，检测血清皮质酮、海马和前额叶皮质（PFC）中 IL-6、TNF-α和 SOD、GPx 水平。CMS 显著增加了皮质酮、IL-6、TNF-α水平，降低了海马和 PFC 中 SOD、GPx 水平（P<0.0001）。与维生素 D 载体处理的大鼠相比，维生素 D 治疗降低了皮质酮水平（P<0.01），增加了 SOD（P<0.0001）和 GPx（P<0.01）水平，降低了海马和 PFC 中 IL-6 和 TNF-α（P<0.0001）水平。维生素 D-10 对 SOD 和 IL-6 水平的调节作用比氟西汀更有效（P<0.0001 和 P<0.01，分别在海马中）。
本研究表明，维生素 D 可有效保护与认知和情感行为相关的大脑关键区域免受慢性应激引起的炎症和氧化应激的影响。
