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母亲怀孕期间过敏与吸烟协同作用,导致成年雄性子代肝纤维化。

Maternal allergy acts synergistically with cigarette smoke exposure during pregnancy to induce hepatic fibrosis in adult male offspring.

机构信息

Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY, USA.

出版信息

J Immunotoxicol. 2011 Oct-Dec;8(4):258-64. doi: 10.3109/1547691X.2011.589412. Epub 2011 Jun 30.

Abstract

Maternal environmental exposures during pregnancy are known to affect disease onset in adult offspring. For example, maternal asthma exacerbations during pregnancy can worsen adult asthma in the offspring. Cigarette smoking during pregnancy is associated with future onset of cardiovascular disease, obesity and diabetes. However, little is known about the effect of maternal environmental exposures on offspring susceptibility to liver disease. This pilot study examined the long-term effect of maternal allergen challenge and/or cigarette smoking during pregnancy on hepatic inflammation and fibrosis in adult mouse offspring. Ovalbumin (OVA) or phosphate-buffered saline (PBS)-sensitized/challenged CD-1 dams were exposed to mainstream cigarette smoke (MCS) or filtered air from gestational day 4 until parturition. Eight weeks postnatally, offspring were sacrificed for comparison of hepatic histology and mRNA expression. Adult male offspring of OVA-sensitized/challenged dams exposed to MCS (OSM) displayed significantly increased liver fibrosis (9.2% collagen content vs. <4% for all other treatment groups). These mice also had 1.8-fold greater collagen 1A1 mRNA levels. From the results here, we concluded that maternal allergen challenge in combination with cigarette smoke exposure during pregnancy may be an important risk factor for liver disease in adult male offspring.

摘要

孕期母体环境暴露已知会影响成年后代疾病的发病。例如,孕期母体哮喘恶化会使后代的成人哮喘加重。孕期吸烟与心血管疾病、肥胖和糖尿病的未来发病有关。然而,对于母体环境暴露对后代肝脏疾病易感性的影响知之甚少。这项初步研究探讨了孕期母体过敏原挑战和/或吸烟对成年小鼠后代肝脏炎症和纤维化的长期影响。卵清蛋白 (OVA) 或磷酸盐缓冲盐水 (PBS)-致敏/挑战的 CD-1 孕鼠从妊娠第 4 天到分娩前暴露于主流香烟烟雾 (MCS) 或过滤空气。产后 8 周,处死后代以比较肝组织学和 mRNA 表达。暴露于 MCS 的 OVA 致敏/挑战孕鼠的成年雄性后代显示出明显增加的肝纤维化(胶原含量为 9.2%,而所有其他治疗组均<4%)。这些小鼠的胶原 1A1 mRNA 水平也增加了 1.8 倍。从这里的结果可以得出结论,孕期母体过敏原挑战与吸烟相结合可能是成年雄性后代肝脏疾病的一个重要危险因素。

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