Evidence Details for
PMID Title Journal Year Abstract
27179524 Effect of Maternal Electroacupuncture on Perinatal Nicotine Exposure-Induced Lung Phenotype in Offspring. Lung. 2016 Aug;194(4):535-46. doi: 10.1007/s00408-016-9899-7. Epub 2016 May 14. 2016 Aug INTRODUCTION: Pregnant women exposed to tobacco smoke predispose the offspring to many adverse consequences including an altered lung development and function. There is no effective therapeutic intervention to block the effects of smoke exposure on the developing lung. Clinical and animal studies demonstrate that acupuncture can modulate a variety of pathophysiological processes, including those involving the respiratory system; however, whether acupuncture affects the lung damage caused by perinatal smoke exposure is not known. METHODS: To determine the effect of acupuncture on perinatal nicotine exposure on the developing lung, pregnant rat dams were administered (1) saline, (2) nicotine, or (3) nicotine + electroacupuncture (EA). Nicotine was administered (1 mg/kg subcutaneously) once a day and EA was applied to both ""Zusanli"" (ST 36) points. Both interventions were administered from gestational day 6 to postnatal day 21 (PND21), following which pups were sacrificed. Lungs, blood, and brain were collected to examine markers of lung injury, repair, and hypothalamic pituitary adrenal (HPA) axis. RESULTS: Concomitant EA application blocked nicotine-induced changes in lung morphology, lung peroxisome proliferator-activated receptor gamma and wingless-int signaling, two key lung developmental signaling pathways, hypothalamic pituitary adrenal axis (hypothalamic corticotropic releasing hormone and lung glucocorticoid receptor levels), and plasma beta-endorphin levels. CONCLUSIONS: Electroacupuncture blocks the nicotine-induced changes in lung developmental signaling pathways and the resultant myogenic lung phenotype, known to be present in the affected offspring. We conclude that EA is a promising novel intervention against the smoke exposed lung damage to the developing lung."

Evidence Sentence: Consistent with the previously published data, perinatal nicotine exposure resulted in decreased PPARgamma signaling, as indicated by decreased PPARgamma (Western analysis and immunostaining) and its downstream target adipocyte differentiation-related protein (ADRP) (Western analysis) levels, and blockage of these changes by the concomitant EA treatment (Fig.
Evidence Sentence: Initially, using lung morphometry, lung PPARgamma and beta-catenin, and BAL SP-A and SP-B protein levels, as markers of lung injury and repair, two subgroups of animals (n=3-4 for each) were used to assess the effect of sham acupuncture (acupuncture using non-acupoints) and EA alone (without nicotine) on lung development,.
Evidence Sentence: Effect of Electroacupuncture on Perinatal Nicotine-Induced Changes in BAL SP-A and SP-B Levels
Evidence Sentence: We next examined SP-A and SP-B levels (ELISA), two well-established lung functional determinants.
Evidence Sentence: Nicotine treatment resulted in a significant increase in BAL SP-A levels, with blockage of this effect in the concomitantly EA-treated group (Fig.
Evidence Sentence: Initially, using lung morphometry, lung PPARgamma and beta-catenin, and BAL SP-A and SP-B protein levels, as markers of lung injury and repair, two subgroups of animals (n=3-4 for each) were used to assess the effect of sham acupuncture (acupuncture using non-acupoints) and EA alone (without nicotine) on lung development,.
Evidence Sentence: Furthermore, perinatal nicotine exposure-induced up-regulation of beta-catenin (Western analysis, immunostaining) and LEF-1 (Western analysis), two key mediators of Wnt signaling, was also blocked in the EA-treated group (Fig.
Evidence Sentence: The blockage of nicotine-induced changes in whole lung PPARgamma and beta-catenin levels was also supported by ELISA (Fig.
Evidence Sentence: Since fetal lung development is driven by HPA axis and acupuncture is known to modulate HPA axis, we next determined hypothalamic CRH and its downstream target relevant for lung development, i.e., lung GR levels.
Evidence Sentence: Compared to the saline only-administered group, hypothalamic CRH content (ELISA) in the nicotine-treated group decreased significantly; however, concomitant EA treatment blocked this decrease (Fig.
Evidence Sentence: Lastly, since CRH regulates beta-endorphin levels, an important marker of body's stress response, which is a key factor in determining lung development and is known to be affected by acupuncture, we next determined the effect of perinatal nicotine exposure and EA on plasma beta-endorphin levels.
Evidence Sentence: In line with the other data on HPA axis (hypothalamic CRH and lung GR levels), concomitant EA administration blocked perinatal nicotine-induced decrease in plasma beta-endorphin levels (Fig.
Evidence Sentence: Concomitant EA application blocked nicotine-induced changes in lung morphology, lung Peroxisome Proliferator-Activated Receptor gamma and Wingless-int signaling, two key lung developmental signaling pathways, hypothalamic pituitary adrenal axis (hypothalamic corticotropic releasing hormone and lung glucocorticoid receptor levels), and plasma beta-endorphin levels.
Evidence Sentence: Since fetal lung development is driven by HPA axis and acupuncture is known to modulate HPA axis, we next determined hypothalamic CRH and its downstream target relevant for lung development, i.e., lung GR levels.
Evidence Sentence: In contrast, lung GR levels increased in the nicotine exposed group, an effect that was also normalized in the EA-treated group (Fig.
Evidence Sentence: In line with the other data on HPA axis (hypothalamic CRH and lung GR levels), concomitant EA administration blocked perinatal nicotine-induced decrease in plasma beta-endorphin levels (Fig.
Evidence Sentence: Furthermore, perinatal nicotine exposure-induced up-regulation of beta-catenin (Western analysis, immunostaining) and LEF-1 (Western analysis), two key mediators of Wnt signaling, was also blocked in the EA-treated group (Fig.
Evidence Sentence: Concomitant EA application blocked nicotine-induced changes in lung morphology, lung Peroxisome Proliferator-Activated Receptor gamma and Wingless-int signaling, two key lung developmental signaling pathways, hypothalamic pituitary adrenal axis (hypothalamic corticotropic releasing hormone and lung glucocorticoid receptor levels), and plasma beta-endorphin levels.
Evidence Sentence: Initially, using lung morphometry, lung PPARgamma and beta-catenin, and BAL SP-A and SP-B protein levels, as markers of lung injury and repair, two subgroups of animals (n=3-4 for each) were used to assess the effect of sham acupuncture (acupuncture using non-acupoints) and EA alone (without nicotine) on lung development,.
Evidence Sentence: Effect of Electroacupuncture on Perinatal Nicotine-Induced Changes in Lung PPARgamma and Wnt signaling
Evidence Sentence: Since the perinatal nicotine-induced lung phenotype has been shown to at least partially result from imbalanced PPARgamma and Wnt signaling, we next probed for key markers of these signaling pathways.
Evidence Sentence: Consistent with the previously published data, perinatal nicotine exposure resulted in decreased PPARgamma signaling, as indicated by decreased PPARgamma (Western analysis and immunostaining) and its downstream target adipocyte differentiation-related protein (ADRP) (Western analysis) levels, and blockage of these changes by the concomitant EA treatment (Fig.
Evidence Sentence: The blockage of nicotine-induced changes in whole lung PPARgamma and beta-catenin levels was also supported by ELISA (Fig.
Evidence Sentence: In fact, as indicated by ELISA, EA not only resulted in blockage of the nicotine-induced decrease in whole lung PPARgamma levels, but resulted in significantly higher levels than the nicotine exposed group.
Evidence Sentence: Initially, using lung morphometry, lung PPARgamma and beta-catenin, and BAL SP-A and SP-B protein levels, as markers of lung injury and repair, two subgroups of animals (n=3-4 for each) were used to assess the effect of sham acupuncture (acupuncture using non-acupoints) and EA alone (without nicotine) on lung development,.
Evidence Sentence: Effect of Electroacupuncture on Perinatal Nicotine-Induced Changes in BAL SP-A and SP-B Levels
Evidence Sentence: We next examined SP-A and SP-B levels (ELISA), two well-established lung functional determinants.
Evidence Sentence: In contrast, the BAL SP-B content in the nicotine exposed group decreased significantly, which was also normalized in the concomitantly EA-treated group (Fig.
Evidence Sentence: Concomitant EA application blocked nicotine-induced changes in lung morphology, lung Peroxisome Proliferator-Activated Receptor gamma and Wingless-int signaling, two key lung developmental signaling pathways, hypothalamic pituitary adrenal axis (hypothalamic corticotropic releasing hormone and lung glucocorticoid receptor levels), and plasma beta-endorphin levels.
Evidence Sentence: Effect of Electroacupuncture on Perinatal Nicotine-Induced Changes in Lung PPARgamma and Wnt signaling
Evidence Sentence: Since the perinatal nicotine-induced lung phenotype has been shown to at least partially result from imbalanced PPARgamma and Wnt signaling, we next probed for key markers of these signaling pathways.
Evidence Sentence: Furthermore, perinatal nicotine exposure-induced up-regulation of beta-catenin (Western analysis, immunostaining) and LEF-1 (Western analysis), two key mediators of Wnt signaling, was also blocked in the EA-treated group (Fig.
Evidence Sentence: The increase in myogenic proteins alpha-SMA and calponin (Western analysis), which is a known consequence of activated Wnt signaling were also blocked by concomitant EA administration (Fig.