Cigarette smoke exposure (SE) during pregnancy is the largest modifiable risk factor for the development of lung disorders in offspring. We have previously shown that maternal L-Carnitine treatment can reduce the adverse impacts of maternal SE on renal and brain disorders in offspring. Here, we investigated the effect of maternal L-Carnitine supplementation on lung inflammatory pathways, autophagy, and mitophagy markers in the offspring in response to maternal SE. Female BALB/c mice (8 weeks) were exposed to cigarette smoke for 6 weeks prior to mating, during gestation and lactation. Some of the SE dams were given L-Carnitine supplementation (1.5 mM in drinking water, SE + LC) during gestation and lactation. Lungs from the offspring were studied at birth and adulthood (13 weeks). At birth, in male offspring, there were increased levels of inflammatory markers (phosphorylated(p)-ERK1,2, p-P38 MAPK, p- NF-κB), and inflammasome marker (NLRP3), as well as mitophagy fission marker Drp-1 and autophagosome marker (LC3A/B-II) in the lung. Maternal L-Carnitine supplementation significantly reduced NLRP3 level. In contrast, maternal SE only increased IL1-β in female offspring, which was reversed by maternal L-Carnitine supplementation. At 13 weeks, there was an increase in LC3A/B-II and p- NF-κB in the male SE offspring with reduced p-JNK1,2, which were partially normalised by maternal L-Carnitine treatment. Female offspring were not affected by maternal SE at this age. Maternal SE had adverse impacts on the male offspring’s lung, which were partially alleviated by maternal L-Carnitine supplementation. Females seem to be less affected by the adverse effects of maternal SE.

中文翻译：

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后代性别影响母体吸烟引起的肺部炎症的易感性和母体抗氧化剂补充剂对小鼠的影响。

怀孕期间的香烟烟雾暴露 (SE) 是后代肺部疾病发展的最大可改变风险因素。我们之前已经表明，母体左旋肉碱治疗可以减少母体 SE 对后代肾脏和脑部疾病的不利影响。在这里，我们研究了母体左旋肉碱补充剂对母体 SE 反应的后代肺部炎症通路、自噬和线粒体标志物的影响。雌性 BALB/c 小鼠（8 周）在交配前、妊娠和哺乳期间暴露于香烟烟雾 6 周。一些 SE 水坝在妊娠和哺乳期间补充了左旋肉碱（饮用水中 1.5 mM，SE + LC）。在出生和成年（13 周）时研究了后代的肺。出生时，在雄性后代中，炎症标志物（磷酸化（p）-ERK1,2、p-P38 MAPK、p-NF-κB）和炎症小体标志物（NLRP3）以及线粒体分裂标志物 Drp-1 和自噬体标志物（LC3A）水平升高/B-II) 在肺中。母体补充左旋肉碱显着降低了 NLRP3 水平。相比之下，母体 SE 仅增加了雌性后代的 IL1-β，而母体补充左旋肉碱则逆转了这种情况。在 13 周时，雄性 SE 后代的 LC3A/B-II 和 p-NF-κB 增加，p-JNK1,2 减少，母体左旋肉碱治疗使这部分正常化。在这个年龄，雌性后代不受母体 SE 的影响。母体 SE 对雄性后代的肺有不利影响，母体​​补充左旋肉碱可部分缓解这种影响。