Abstract：
Ulcerative colitis (UC) is an inflammatory condition that affects the colon\'s lining and increases the risk of colon cancer. Despite ongoing research, there is no identified cure for UC. The recognition of NLRP3 inflammasome activation in the pathogenesis of UC has gained widespread acceptance. Notably, the ketone body β-hydroxybutyrate inhibits NLRP3 demonstrating its anti-inflammatory properties. Additionally, BD-AcAc 2 is ketone mono ester that increases β-hydroxybutyrate blood levels. It has the potential to address the constraints associated with exogenous β-hydroxybutyrate as a therapeutic agent, including issues related to stability and short duration of action. However, the effects of β-hydroxybutyrate and BD-AcAc 2 on colitis have not been fully investigated. This study found that while both exogenous β-hydroxybutyrate and BD-AcAc 2 produced the same levels of plasma β-hydroxybutyrate, BD-AcAc 2 demonstrated superior effectiveness in mitigating dextran sodium sulfate-induced UC in rats. The mechanism of action involves modulating the NF-κB signaling, inhibiting the NLRP3 inflammasome, regulating antioxidant capacity, controlling tight junction protein expression and a potential to inhibit apoptosis and pyroptosis. Certainly, BD-AcAc 2\'s anti-inflammatory effects require more than just increasing plasma β-hydroxybutyrate levels and other factors contribute to its efficacy. Local ketone concentrations in the gastrointestinal tract, as well as the combined effect of specific ketone bodies, are likely to have contributed to the stronger protective effect observed with ketone mono ester ingestion in our experiment. As a result, further investigations are necessary to fully understand the mechanisms of BD-AcAc 2 and optimize its use.
摘要：
溃疡性结肠炎（UC）是一种影响结肠内膜并增加结肠癌风险的炎症。尽管正在进行研究，没有确定的治疗UC。NLRP3炎性体激活在UC发病机制中的认识已获得广泛接受。值得注意的是,酮体β-羟基丁酸酯抑制NLRP3,表明其抗炎特性。此外,BD-AcAc2是增加β-羟基丁酸酯血液水平的酮单酯。它有可能解决与外源性β-羟基丁酸酯作为治疗剂相关的限制，包括与稳定性和行动持续时间短有关的问题。然而,β-羟基丁酸酯和BD-AcAc2对结肠炎的作用尚未得到充分研究.这项研究发现，虽然外源β-羟基丁酸酯和BD-AcAc2产生相同水平的血浆β-羟基丁酸酯，BD-AcAc2在减轻葡聚糖硫酸钠诱导的大鼠UC方面表现出优异的有效性。作用机制涉及调节NF-κB信号,抑制NLRP3炎性体，调节抗氧化能力，控制紧密连接蛋白的表达和抑制细胞凋亡和焦亡的潜力。当然,BD-AcAc2的抗炎作用不仅仅需要增加血浆β-羟基丁酸酯水平，其他因素也有助于其疗效。胃肠道中的局部酮浓度，以及特定酮体的联合作用，在我们的实验中，可能对酮单酯摄入观察到的更强的保护作用做出了贡献。因此,进一步的研究是必要的，以充分了解BD-AcAc2的机制和优化其使用。
