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首页> 外文期刊>International Journal of Molecular Sciences >Maternal Tryptophan Supplementation Protects Adult Rat Offspring against Hypertension Programmed by Maternal Chronic Kidney Disease: Implication of Tryptophan-Metabolizing Microbiome and Aryl Hydrocarbon Receptor
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Maternal Tryptophan Supplementation Protects Adult Rat Offspring against Hypertension Programmed by Maternal Chronic Kidney Disease: Implication of Tryptophan-Metabolizing Microbiome and Aryl Hydrocarbon Receptor

机译：母体色氨酸补充剂保护成人大鼠后代对母慢性肾病编程的高血压：色氨酸代谢微生物组和芳基烃受体的含义

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Hypertension and chronic kidney disease (CKD) can originate during early-life. Tryptophan metabolites generated by different pathways have both detrimental and beneficial effects. In CKD, uremic toxins from the tryptophan-generating metabolites are endogenous ligands of the aryl hydrocarbon receptor (AHR). The interplay between AHR, nitric oxide (NO), the renin–angiotensin system (RAS), and gut microbiota is involved in the development of hypertension. We examined whether tryptophan supplementation in pregnancy can prevent hypertension and kidney disease programmed by maternal CKD in adult offspring via the aforementioned mechanisms. Sprague–Dawley (SD) female rats received regular chow or chow supplemented with 0.5% adenine for 3 weeks to induce CKD before pregnancy. Pregnant controls or CKD rats received vehicle or tryptophan 200 mg/kg per day via oral gavage during pregnancy. Male offspring were divided into four groups ( n = 8/group): control, CKD, tryptophan supplementation (Trp), and CKD plus tryptophan supplementation (CKDTrp). All rats were sacrificed at the age of 12 weeks. We found maternal CKD induced hypertension in adult offspring, which tryptophan supplementation prevented. Maternal CKD-induced hypertension is related to impaired NO bioavailability and non-classical RAS axis. Maternal CKD and tryptophan supplementation differentially shaped distinct gut microbiota profile in adult offspring. The protective effect of tryptophan supplementation against maternal CKD-induced programmed hypertension is relevant to alterations to several tryptophan-metabolizing microbes and AHR signaling pathway. Our findings support interplay among tryptophan-metabolizing microbiome, AHR, NO, and the RAS in hypertension of developmental origins. Furthermore, tryptophan supplementation in pregnancy could be a potential approach to prevent hypertension programmed by maternal CKD.
机译：高血压和慢性肾病（CKD）在早期期间可以发起。由不同途径产生的色氨酸代谢物具有不利和有益的效果。在CKD中，来自色氨酸产生代谢物的尿毒性毒素是芳基烃受体（AHR）的内源性配体。 AHR，一氧化氮（NO），肾素 - 血管紧张素系统（RAS）和肠道微生物会之间的相互作用参与高血压的发育。我们检查了妊娠中的色氨酸补充剂是否可以通过上述机制预防成人后代母体CKD的高血压和肾病。 Sprague-Dawley（SD）雌性大鼠在怀孕前3周接受了第3周的常规食物或食物，患有0.5％的腺嘌呤，以诱导妊娠前CKD。怀孕期间，孕妇对照或CKD大鼠通过口服饲喂载体或每天红耳果/千克/千克。雄性后代分为四组（n = 8 /组）：对照，CKD，色氨酸补充（TRP）和CKD加色氨酸补充（CKDTRP）。所有大鼠在12周龄均处死。我们发现母亲CKD诱导的成人后代高血压，这是一种试用的色氨酸补充剂。母性CKD诱导的高血压与损害有关，没有生物利用度和非典型的RAS轴。母体CKD和色氨酸补充剂在成人后代中的差异形状不同的肠道微生物血管谱。 CKD诱导的母性CKD诱导的编程高血压的特性对母性CKD诱导的细胞型高血压的保护作用与几种色氨酸代谢微生物和AHR信号通路的改变有关。我们的研究结果支持在发育起源高血压中的色氨酸代谢微生物组，AHR，NO和RA之间的相互作用。此外，怀孕的色氨酸补充剂可能是预防母婴编程的高血压的潜在方法。

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