Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy.
Department of Pharmacological and Physiological Science, Saint Louis University, St. Louis, MO 63103, USA.
Int J Mol Sci. 2020 Apr 24;21(8):3026. doi: 10.3390/ijms21083026.
The major end-products of dietary fiber fermentation by gut microbiota are the short-chain fatty acids (SCFAs) acetate, propionate, and butyrate, which have been shown to modulate host metabolism via effects on metabolic pathways at different tissue sites. Several studies showed the inhibitory effects of sodium propionate (SP) on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. We carried out an in vitro model of inflammation on the J774-A1 cell line, by stimulation with lipopolysaccharide (LPS) and HO, followed by the pre-treatment with SP at 0.1, 1 mM and 10 mM. To evaluate the effect on acute inflammation and superoxide anion-induced pain, we performed a model of carrageenan (CAR)-induced rat paw inflammation and intraplantar injection of KO where rats received SP orally (10, 30, and 100 mg/kg). SP decreased in concentration-dependent-manner the expression of cicloxigenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) following LPS stimulation. SP was able to enhance anti-oxidant enzyme production such as manganese superoxide dismutase (MnSOD) and heme oxygenase-1 (HO-1) following HO stimulation. In in vivo models, SP (30 and 100 mg/kg) reduced paw inflammation and tissue damage after CAR and KO injection. Our results demonstrated the anti-inflammatory and anti-oxidant properties of SP; therefore, we propose that SP may be an effective strategy for the treatment of inflammatory diseases.
膳食纤维在肠道菌群作用下的主要终产物是短链脂肪酸（SCFAs），包括乙酸盐、丙酸盐和丁酸盐。这些短链脂肪酸通过对不同组织部位代谢途径的影响来调节宿主代谢。几项研究表明丙酸钠（SP）对核因子 kappa-轻链增强子的 B 细胞（NF-κB）通路有抑制作用。我们在 J774-A1 细胞系上进行了炎症的体外模型实验，通过脂多糖（LPS）和 HO 刺激，然后用 0.1、1mM 和 10mM 的 SP 预处理。为了评估其对急性炎症和超氧阴离子诱导疼痛的影响，我们进行了角叉菜胶（CAR）诱导的大鼠足肿胀炎症模型和腹腔内注射 KO 的实验，其中大鼠口服给予 SP（10、30 和 100mg/kg）。SP 以浓度依赖性方式降低 LPS 刺激后环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的表达。SP 能够增强 HO 刺激后的抗氧化酶产生，如锰超氧化物歧化酶（MnSOD）和血红素加氧酶-1（HO-1）。在体内模型中，SP（30 和 100mg/kg）可减轻 CAR 和 KO 注射后的足肿胀和组织损伤。我们的结果表明 SP 具有抗炎和抗氧化特性；因此，我们提出 SP 可能是治疗炎症性疾病的有效策略。
