Abstract
Introduction. Environmental exposure of the developing offspring to cigarette smoke or nicotine is an important predisposing factor for many chronic respiratory conditions, such as asthma, emphysema, pulmonary fibrosis, and so forth, in the exposed offspring. Studies showed that electroacupuncture (EA) applied to maternal “Zusanli” (ST36) acupoints during pregnancy and lactation protects against perinatal nicotine exposure- (PNE-) induced lung damage. However, the most effective time period, that is, prenatal vs. postnatal, to attain this effect has not been determined. Objective To determine the most effective developmental timing of EA's protective effect against PNE-induced lung phenotype in the exposed offspring. Methods Pregnant rats were given (1) saline (“S” group); (2) nicotine (“N” group); (3) nicotine + EA, exclusively prenatally (“Pre-EA” group); (4) nicotine + EA, exclusively postnatally (“Post-EA,” group); and (5) nicotine + EA, administered both prenatally and postnatally (“Pre- and Post-EA” group). Nicotine was injected once daily (1 mg/kg, 100 μl) and EA was administered to bilateral ST36 acupoints once daily during the specified time-periods. At the end of the experimental periods, key hypothalamic pituitary adrenal (HPA) axis markers in pups and dams, and lung function, morphometry, and the central molecular markers of lung development in the offspring were determined. Results After nicotine exposure, alveolar mean linear intercept (MLI) increased, but mean alveolar number (MAN) decreased and lung PPARγ level decreased, but glucocorticoid receptor (GR) and serum corticosterone (Cort) levels increased, in line with the known PNE-induced lung phenotype. In the nicotine exposed group, maternal hypothalamic corticotropin releasing hormone (CRH) level decreased, but pituitary adrenocorticotropic hormone (ACTH) and serum Cort levels increased. In the “Pre- and Post-EA” groups, PNE-induced alterations in lung morphometry, lung development markers, and HPA axis were blocked. In the “Pre-EA” group, PNE-induced changes in lung morphometry, GR, and maternal HPA axis improved; lung PPARγ level decreased, but glucocorticoid receptor (GR) and serum corticosterone (Cort) levels increased, in line with the known PNE-induced lung phenotype. In the nicotine exposed group, maternal hypothalamic corticotropin releasing hormone (CRH) level decreased, but pituitary adrenocorticotropic hormone (ACTH) and serum Cort levels increased. In the “Pre- and Post-EA” groups, PNE-induced alterations in lung morphometry, lung development markers, and HPA axis were blocked. In the “Pre-EA” group, PNE-induced changes in lung morphometry, GR, and maternal HPA axis improved; lung PPARConclusions Maternal EA applied to ST36 acupoints during both pre- and postnatal periods preserves offspring lung structure and function despite perinatal exposure to nicotine. EA applied during the “prenatal period” affords only limited benefits, whereas EA applied during the “postnatal period” is ineffective, suggesting that the EA's effects in modulating PNE-induced lung phenotype are limited to specific time-periods during lung development.
Highlights
Environmental exposure of the developing offspring to cigarette smoke or nicotine is an important predisposing factor for many chronic respiratory conditions, such as asthma, emphysema, pulmonary fibrosis, and so forth, in the exposed offspring
Its effects are especially pronounced on the developing lung [11], as it predisposes the exposed offspring to many chronic respiratory conditions such as asthma, emphysema, pulmonary fibrosis, and so forth. [12,13,14,15]. ese effects appear to be permanent, lasting to adulthood and some can even be potentially transmitted to future generations [16, 17]
By comparing EA’s protective effects against nicotine-induced lung phenotype, administered exclusively during the “prenatal period”, “postnatal period”, or both “prenatal and postnatal periods”, we found that the perinatal nicotine exposure- (PNE-)induced lung morphometric (MLI and mean alveolar number (MAN)) and functional (Cdyn, peak expiratory flow (PEF), minute ventilation volume (MV), and RL) changes were effectively blocked only when EA was administered during both “prenatal and postnatal periods.” is is in line with our previous findings [31, 32]
Summary
Environmental exposure of the developing offspring to cigarette smoke or nicotine is an important predisposing factor for many chronic respiratory conditions, such as asthma, emphysema, pulmonary fibrosis, and so forth, in the exposed offspring. To determine the most effective developmental timing of EA’s protective effect against PNE-induced lung phenotype in the exposed offspring. In the “Pre-EA” group, PNE-induced changes in lung morphometry, GR, and maternal HPA axis improved; lung PPARc and serum Cort levels were slightly but not significantly improved. Maternal EA applied to ST36 acupoints during both pre- and postnatal periods preserves offspring lung structure and function despite perinatal exposure to nicotine. Its effects are especially pronounced on the developing lung [11], as it predisposes the exposed offspring to many chronic respiratory conditions such as asthma, emphysema, pulmonary fibrosis, and so forth. Its effects are especially pronounced on the developing lung [11], as it predisposes the exposed offspring to many chronic respiratory conditions such as asthma, emphysema, pulmonary fibrosis, and so forth. [12,13,14,15]. ese effects appear to be permanent, lasting to adulthood and some can even be potentially transmitted to future generations [16, 17]
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