Neonatal sepsis (NS) is a severe syndrome in newborns that is induced by infections, and the initiation and development of NS are closely associated with the function of miRs. In the current study, the effects of berberine, which is a functional component in traditional Chinese medicine (TCM), against NS were assessed by focusing on the interaction of berberine with miR-132-3p-mediated signaling. An NS model was induced using cecal slurry (CS) in vivo and LPS in vitro, and berberine treatment was applies. The changes in survival rate, intestinal structure, and systemic inflammation in mice and the viability, apoptosis, and inflammatory response in intestinal cells were measured. At the molecular level, miR-132-3p levels and the activities of the FOXA1 and NF-κB pathways were analyzed. The data showed that berberine increased the survival rates of CS-induced mice. The intestinal injuries induced by CS were also attenuated by berberine, which was associated with inhibition of the production of systemic IL-6, IL-1β, and TNF-α. At the molecular level, the expression of miR-132-3p was upregulated, suppressing the expression of FOXA1, p-IκBα, and p65 while inducing the expression of IκBα. The effects of berberine on NS-induced impairments were blocked by the injection of the miR-132-3p antagomir, which exacerbated intestinal injuries, induced systemic inflammation, and reactivated the FOXA1 and NF-κB pathways. The findings in the in vivo model were validated with in vitro assays. Collectively, the findings outlined in the current study indicated that berberine had solid protective effects against NS-induced symptoms in newborn mice, and the effects depended on the upregulation of miR-132-3p.

新生儿败血症（NS）是由感染引起的新生儿严重综合征，NS的发生和发展与miRs的功能密切相关。在目前的研究中，通过关注小檗碱与 miR-132-3p 介导的信号传导的相互作用，评估了作为中药 (TCM) 功能成分的黄连素对 NS 的作用。使用体内盲肠浆（CS）和体外LPS诱导NS模型，并应用小檗碱处理。测量小鼠存活率、肠道结构和全身炎症的变化以及肠道细胞的活力、凋亡和炎症反应。在分子水平上，分析了 miR-132-3p 水平以及 FOXA1 和 NF-κB 通路的活性。数据显示，小檗碱提高了 CS 诱导小鼠的存活率。小檗碱也可减轻 CS 引起的肠道损伤，这与抑制全身性 IL-6、IL-1β 和 TNF-α 的产生有关。在分子水平上，miR-132-3p的表达上调，抑制FOXA1、p-IκBα和p65的表达，同时诱导IκBα的表达。注射 miR-132-3p antagomir 可阻断小檗碱对 NS 引起的损伤的影响，这会加剧肠道损伤，诱发全身炎症，并重新激活 FOXA1 和 NF-κB 通路。体内模型中的发现通过体外测定得到验证。总的来说，当前研究中概述的研究结果表明，小檗碱对新生小鼠 NS 诱导的症状具有坚实的保护作用，