Premium
Effect of electro‐acupuncture at ST 36 on maternal food restriction‐induced lung phenotype in rat offspring
Author(s) -
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.
Publication year - 2021
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.25466
Subject(s) - offspring , medicine , lung , pregnancy , zusanli , bronchopulmonary dysplasia , endocrinology , nicotine , phenotype , fetus , pathology , acupuncture , biology , genetics , gestational age , alternative medicine , electroacupuncture , gene
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.