A topic dermatitis (AD) is a common chronic and recurrent skin disorder. The protective effects of sodium butyrate (NaB), a metabolite of short-chain fatty acid breakdown by the gut microbiota, have been widely reported in numerous inflammatory diseases. However, the effect of NaB treatment alone on AD has not been reported. In the current study, AD was induced in BALB/c mice with 2,4-dinitrochlorobenzene (DNCB) for 28 days with NaB (200 mg/kg) treatment by gavage. NaB attenuated AD-induced skin bleeding, scarring, dryness, abrasions and erosions. In addition, NaB inhibited inflammatory cells infiltration and attenuated the expression of inflammatory cytokines and chemokines. Mechanistically, NaB reduced histone deacetylase 3 (HDAC3) expression and NF-κB p65 nuclear translocation by increasing the lysine acetylation levels of STAT1 and NF-κB p65 in AD. Taken together, our study suggests that NaB inhibits inflammatory mediators and ameliorates AD by inhibiting HDAC3 expression, thereby upregulating STAT1 and NF-κB p65 lysine acetylation levels and reducing NF-κB p65 nuclear translocation. Therefore, this study provides a new theoretical basis for NaB in the treatment of AD.

局部皮炎（AD）是一种常见的慢性、复发性皮肤病。丁酸钠 (NaB) 是肠道微生物群分解短链脂肪酸的代谢产物，其在多种炎症性疾病中的保护作用已被广泛报道。然而，NaB单独治疗对AD的效果尚未见报道。在当前的研究中，用 2,4-二硝基氯苯 (DNCB) 和 NaB (200 mg/kg) 灌胃法治疗 BALB/c 小鼠 28 天，诱导 AD。NaB 可减轻 AD 引起的皮肤出血、疤痕、干燥、擦伤和糜烂。此外，NaB 抑制炎症细胞浸润并减弱炎症细胞因子和趋化因子的表达。从机制上讲，NaB 通过增加 AD 中 STAT1 和 NF-κB p65 的赖氨酸乙酰化水平来减少组蛋白脱乙酰酶 3 (HDAC3) 表达和 NF-κB p65 核转位。综上所述，我们的研究表明 NaB 通过抑制 HDAC3 表达来抑制炎症介质并改善 AD，从而上调 STAT1 和 NF-κB p65 赖氨酸乙酰化水平并减少 NF-κB p65 核转位。因此，本研究为NaB治疗AD提供了新的理论依据。