Long-term consequences of stress intervene in normal signaling of the brain leading to many psychological complications. The enriched environment (EE) may potentially ameliorate the stress response in rats. However, the mechanistic understanding of the enriched environment in protecting the myelin membrane from oxidative damage after prolonged exposure to immobilization stress (IS) remains vague. In the current study, we examined the impact of EE by exposing the rats to IS (4 h/day) followed by EE treatment (2 h/day) for 28 days and the activities of ROS, lipid peroxides, and phospholipids were studied, and its influence on the myelin regulatory factor (MyRF) and enzymes linked to sphingolipid was assessed in the forebrain region of myelin membrane. The ROS and lipid peroxidation was increased, and a significant decrease in the antioxidant activities was found in the IS group. IS + EE could reduce oxidative damage and increase the levels of antioxidant activities. The individual phospholipids including sphingomyelin (SM), phosphatidylcholine (PC), phosphatidylinositol (PI), phosphatidylserine (PS), phosphatidylethanolamine (PE), and phosphatidic acid (PA) were decreased in the IS group, while IS + EE exhibited significant increase in the phospholipid classes regardless of the exposure to IS. There was down-regulation in the mRNA levels of MyRF, CERS2, SPLTC2, UGT8, and GLTP, while IS + EE could mitigate the up-regulation in the levels of mRNA of MyRF, CERS2, SPLTC2, UGT8, and GLTP. The protein expression of MOG, PLP1, and mTOR was found to be reduced in the IS group of rats, however, IS + EE revealed significant increase in the expression of these signaling molecules. These results suggest that EE had a positive effect on chronic stress response by protecting the myelin membrane against oxidative damage and increasing the protein synthesis required for myelin membrane plasticity via activation of MyRF and mTOR signaling in the forebrain region of IS exposed rats.

压力的长期后果会干扰大脑的正常信号传导，导致许多心理并发症。丰富的环境（EE）可能会改善大鼠的应激反应。然而，对于长期暴露于固定应激（IS）后富集环境保护髓磷脂膜免受氧化损伤的机制理解仍然模糊。在当前的研究中，我们通过将大鼠暴露于 IS（4 小时/天），然后进行 EE 治疗（2 小时/天）28 天来检查 EE 的影响，并研究了 ROS、脂质过氧化物和磷脂的活性，并在髓磷脂膜的前脑区域评估了它对髓磷脂调节因子（MyRF）和与鞘脂相关的酶的影响。ROS和脂质过氧化增加，IS组的抗氧化活性显着下降。IS + EE 可以减少氧化损伤并提高抗氧化活性水平。IS组中的个别磷脂包括鞘磷脂(SM)、磷脂酰胆碱(PC)、磷脂酰肌醇(PI)、磷脂酰丝氨酸(PS)、磷脂酰乙醇胺(PE)和磷脂酸(PA)在IS组中下降，而IS+EE则表现出显着增加。磷脂类别与暴露于 IS 无关。出现了下调 IS 组中磷脂酸 (PA) 和磷脂酸 (PA) 下降，而 IS + EE 的磷脂类别显着增加，无论暴露于 IS 的情况如何。出现了下调 IS 组中磷脂酸 (PA) 和磷脂酸 (PA) 下降，而 IS + EE 的磷脂类别显着增加，无论暴露于 IS 的情况如何。出现了下调MyRF、CERS2、SPLTC2、UGT8和GLTP的mRNA水平，而 IS + EE 可以减轻MyRF、CERS2、SPLTC2、UGT8和GLTP mRNA水平的上调。IS组大鼠中MOG、PLP1和mTOR的蛋白表达减少，但IS + EE显示这些信号分子的表达显着增加。这些结果表明，EE 通过保护髓磷脂膜免受氧化损伤并通过激活 IS 暴露大鼠前脑区域的 MyRF 和 mTOR 信号来增加髓磷脂膜可塑性所需的蛋白质合成，从而对慢性应激反应产生积极影响。