Mou Qiujie, Ji Bo, Zhao Guozhen, Liu Yitian, Sakurai Reiko, Xie Yana, Zhang Qin, Dai Jian, Lu Yawen, Ge Yunpeng, Shi Tianyu, Xu Shuang, Rehan Virender K
Beijing University of Chinese Medicine, Beijing, China.
Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing, China.
Pediatr Pulmonol. 2021 Aug;56(8):2537-2545. doi: 10.1002/ppul.25466. Epub 2021 May 25.
Maternal food restriction (MFR) during pregnancy leads to pulmonary dysplasia in the newborn period and increases susceptibility to diseases, such as asthma and chronic lung disease, later in life. Previous studies have shown that maternal electro-acupuncture (EA) applied to "Zusanli" (ST 36) could prevent the abnormal expression of key lung developmental signaling pathways and improve the lung morphology and function in perinatal nicotine exposed offspring. There is a significant overlap in lung developmental signaling pathways affected by perinatal nicotine exposure and MFR during pregnancy; however, whether maternal EA at ST 36 also blocks the MFR-induced lung phenotype is unknown. Here, we examined the effects of EA applied to maternal ST 36 on lung morphology and function and the expression of key lung developmental signaling pathways, and the hypercorticoid state associated with MFR during pregnancy. These effects were compared with those of metyrapone, an intervention known to block MFR-induced offspring hypercorticoid state and the resultant pulmonary pathology. Like metyrapone, maternal EA at ST 36 blocked the MFR-induced changes in key developmental signaling pathways and protected the MFR-induced changes in lung morphology and function. These results offer a novel and safe, nonpharmacologic approach to prevent MFR-induced pulmonary dysplasia in offspring.
孕期母体食物限制(MFR)会导致新生儿期肺发育不良,并增加其日后患哮喘和慢性肺病等疾病的易感性。先前的研究表明,对母体“足三里”(ST 36)进行电针治疗可防止围产期尼古丁暴露后代关键肺发育信号通路的异常表达,并改善其肺形态和功能。围产期尼古丁暴露和孕期MFR所影响的肺发育信号通路存在显著重叠;然而,对母体ST 36进行电针治疗是否也能阻止MFR诱导的肺表型尚不清楚。在此,我们研究了对母体ST 36进行电针治疗对肺形态和功能、关键肺发育信号通路表达以及孕期与MFR相关的高皮质醇状态的影响。将这些影响与甲吡酮的影响进行了比较,甲吡酮是一种已知可阻止MFR诱导的后代高皮质醇状态及由此产生的肺部病变的干预措施。与甲吡酮一样,对母体ST 36进行电针治疗可阻止MFR诱导的关键发育信号通路变化,并保护MFR诱导的肺形态和功能变化。这些结果为预防MFR诱导的后代肺发育不良提供了一种新颖、安全的非药物方法。