2014
DOI: 10.1002/bdrb.21092
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4‐O‐methylhonokiol Inhibits Serious Embryo Anomalies Caused by Nicotine via Modulations of Oxidative Stress, Apoptosis, and Inflammation

Abstract: These findings indicate that 4-O-methylhonokiol reduces serious embryo anomalies caused by nicotine in mouse embryos via the modulations of oxidative stress, apoptosis, and inflammation, suggesting that 4-O-methylhonokiol may be a preventive and therapeutic agent against the dysmorphology induced by maternal smoking during pregnancy.

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Cited by 14 publications
(10 citation statements)
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“…This response could alter signal transduction pathways, damage macro-molecules, produce vasoactive compounds (e.g., isoprostanes), alter both placental morphology (e.g., placental calcification) and blood flow, and contribute to intrauterine growth retardation and low birth weight (Hutter et al 2010; Stone et al 2014). Additional evidence suggests the possibility of inflammatory pathways (Lin et al 2014; Pringle et al 2015) and epigenetic modifications (Knopik et al 2012), but the mechanisms by which these effects are transmitted is poorly understood. Considerably more research, particularly prospective, genetically informed, and carefully designed animal and human studies that can address critical/sensitive periods of exposure, measurements or biomarkers of exposure effects (e.g., placental tissue) and longitudinal course of disease and behavior is needed to begin to disentangle the likely complex nature of this association.…”
Section: Discussionmentioning
confidence: 99%
“…This response could alter signal transduction pathways, damage macro-molecules, produce vasoactive compounds (e.g., isoprostanes), alter both placental morphology (e.g., placental calcification) and blood flow, and contribute to intrauterine growth retardation and low birth weight (Hutter et al 2010; Stone et al 2014). Additional evidence suggests the possibility of inflammatory pathways (Lin et al 2014; Pringle et al 2015) and epigenetic modifications (Knopik et al 2012), but the mechanisms by which these effects are transmitted is poorly understood. Considerably more research, particularly prospective, genetically informed, and carefully designed animal and human studies that can address critical/sensitive periods of exposure, measurements or biomarkers of exposure effects (e.g., placental tissue) and longitudinal course of disease and behavior is needed to begin to disentangle the likely complex nature of this association.…”
Section: Discussionmentioning
confidence: 99%
“…Anatomopathological studies of umbilical cords and placentas of newborn infants from mothers who are smokers demonstrate that tobacco increases the release of vasoactive substances and decreases the release of vasodilator substances such as nitric oxide (NO) [ 47 , 48 ], contributing further to oxidative stress, shear stress, hypoxia and inflammation [ 13 , 49 ]. Based on a large number of studies in animal models, these four types of stimuli can drive a compensatory adaptive structural change known as outward vascular remodeling [ 50 - 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…It has become evident that oxidative stress is one of the most important mechanisms involved in tobacco smoking during pregnancy [ 6 , 10 , 12 , 13 ]. The increase in reactive oxygen species (ROS) production from exogenous and endogenous sources results in an imbalance between the generation of oxidant species and antioxidant defenses [ 14 - 16 ].…”
Section: Introductionmentioning
confidence: 99%
“…Rodents exposed to nicotine in utero had significantly increased circulating serum pro-inflammatory cytokines (e.g., IL1b, IL6, and TNFa) throughout early development and adulthood (Mohsenzadeh et al 2014, Orellana et al 2014. Similarly, embryos exposed to nicotine had increased gene expression of TNFa and IL1b (Lin et al 2014). Importantly, these cytokines play key roles in germ cell survival and gonadal steroidogenesis (Bornstein et al 2004, Perez et al 2013, Field et al 2014.…”
Section: The Role Of Inflammationmentioning
confidence: 99%