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Developmental Timing Determines the Protective Effect of Maternal Electroacupuncture on Perinatal Nicotine
Jian Dai1, Bo Ji1, Guozhen Zhao1
1School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China.
Insights
Electroacupuncture (EA) during both prenatal and postnatal periods best protects offspring lungs from nicotine damage. Prenatal EA offers limited benefits, while postnatal EA is ineffective in preventing lung damage from perinatal nicotine exposure (PNE).
Area of Science:
- Developmental toxicology
- Respiratory medicine
- Integrative medicine
Background:
- Perinatal nicotine exposure (PNE) is a significant risk factor for chronic respiratory conditions in offspring.
- Electroacupuncture (EA) at the ST36 acupoint shows promise in mitigating PNE-induced lung damage.
- The optimal timing for EA intervention (prenatal vs. postnatal) remains undetermined.
Purpose of the Study:
- To ascertain the most effective developmental timing for EA's protective effects against PNE-induced lung abnormalities.
- To evaluate the impact of prenatal, postnatal, and combined prenatal/postnatal EA on offspring lung development following PNE.
Main Methods:
- Pregnant rats were divided into groups receiving saline, nicotine, or nicotine plus EA during specific prenatal and/or postnatal periods.
- EA was applied to bilateral ST36 acupoints daily.
- Offspring lung function, morphometry, and hypothalamic-pituitary-adrenal (HPA) axis markers were assessed.
Main Results:
- PNE led to increased lung alveolar mean linear intercept (MLI), decreased mean alveolar number (MAN), and altered lung molecular markers (PPARγ, GR).
- Combined prenatal and postnatal EA (Pre- and Post-EA) effectively blocked PNE-induced lung and HPA axis disturbances.
- Prenatal EA (Pre-EA) partially improved lung morphometry and maternal HPA axis function but did not fully restore lung markers.
Conclusions:
- Maternal EA at ST36 acupoints during both prenatal and postnatal periods is crucial for preserving offspring lung structure and function following PNE.
- Prenatal EA provides limited protection, and postnatal EA alone is ineffective.
- The protective efficacy of EA against PNE-induced lung phenotypes is time-sensitive, highlighting critical developmental windows.
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 PPAR.
Conclusions:
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.
