School of Nursing, Capital Medical University, Beijing, China.
China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Environ Sci Pollut Res Int. 2022 Oct;29(49):74851-74860. doi: 10.1007/s11356-022-21102-3. Epub 2022 Jun 1.
We have previously reported that filtered air (FA) intervention reduces inflammation and hypothalamus-pituitary-adrenal axis activation after fine particulate matter (PM2.5 exposure). Whether FA also modulates the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-gonadal (HPG) axes in rats after PM2.5 exposure is still unknown. Adult Sprague-Dawley rats were exposed to PM2.5 by using a "real-world" PM2.5 exposure system, and the FA intervention was conducted by renewing for 15 days. PM2.5 inhalation decreased thyrotropin-releasing hormone (TRH) and thyroxine (T4) levels in both male and female rats, and thyroid-stimulating hormone (TSH) level in male rats. FA intervention attenuated the reduction in TRH and TSH levels in male rats and reduction in T4 level in female rats. PM2.5 inhalation also reduced testosterone (T) level in male rats, and estradiol (E2) and progesterone (PROG) levels in female rats, and these changes were attenuated after FA intervention. The FA intervention attenuated the decreases in CD8 T cells and T cells induced by PM2.5 inhalation in female rats only by flow cytometry analysis. In blood, FA interventions ameliorated IL-6 and IL-1β mRNA levels in both male and female rats after PM2.5 exposure. FA intervention restored the IL-4 and IL-10 levels in female rats after PM2.5 exposure. Moreover, FA intervention ameliorated the inflammatory responses induced by PM2.5 inhalation in the thyroid and gonads in both male and female rats. These data indicate that FA intervention exerted an effect on modulating the hormonal balance of the HPT and HPG axes, and this may be related to a reduction in the inflammatory responses in the thyroid and gonads of PM2.5-treated rats, respectively.
我们之前的研究表明，空气过滤干预可减轻细颗粒物（PM2.5）暴露后炎症和下丘脑-垂体-肾上腺轴（HPA）的激活。然而，空气过滤是否也能调节 PM2.5 暴露后大鼠的下丘脑-垂体-甲状腺（HPT）和下丘脑-垂体-性腺（HPG）轴尚不清楚。成年 Sprague-Dawley 大鼠通过使用“真实世界”PM2.5 暴露系统暴露于 PM2.5，空气过滤干预持续 15 天。PM2.5 吸入降低了雌雄大鼠的促甲状腺激素释放激素（TRH）和甲状腺素（T4）水平，以及雄性大鼠的促甲状腺激素（TSH）水平。空气过滤干预减弱了雄性大鼠 TRH 和 TSH 水平的降低以及雌性大鼠 T4 水平的降低。PM2.5 吸入还降低了雄性大鼠的睾酮（T）水平和雌性大鼠的雌二醇（E2）和孕酮（PROG）水平，空气过滤干预减弱了这些变化。通过流式细胞术分析，空气过滤干预仅减弱了 PM2.5 吸入引起的雌性大鼠 CD8 T 细胞和 T 细胞的减少。在血液中，空气过滤干预改善了 PM2.5 暴露后雌雄大鼠的 IL-6 和 IL-1β mRNA 水平。空气过滤干预恢复了 PM2.5 暴露后雌性大鼠的 IL-4 和 IL-10 水平。此外，空气过滤干预改善了雌雄大鼠甲状腺和性腺中 PM2.5 吸入引起的炎症反应。这些数据表明，空气过滤干预对调节 HPT 和 HPG 轴的激素平衡具有一定的作用，这可能与 PM2.5 处理大鼠甲状腺和性腺中的炎症反应减少有关。
