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辛酸钠通过改变肠道微生物代谢来改善肠道黏膜屏障功能和抗氧化能力。

Sodium caprylate improves intestinal mucosal barrier function and antioxidant capacity by altering gut microbial metabolism.

机构信息

State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing, China.

出版信息

Food Funct. 2021 Oct 19;12(20):9750-9762. doi: 10.1039/d1fo01975a.

Abstract

Short-chain fatty acids (SCFA) produced by gut microbial metabolism have been reported to regulate the immunological response and intestinal health of the host by activating G protein-coupled receptors (GPR). It is unclear whether medium-chain fatty acids (MCFA) improve the intestinal barrier function by activating GPR. This study was conducted to investigate the effects of sodium caprylate and sodium butyrate on antioxidant capacity and intestinal barrier function in IPEC-J2 treated with HO and C57/BL6 mouse models. For and assays, mice and oxidation-damaged IPEC-J2 (NC) were treated with sodium caprylate (SC) and sodium butyrate (PC) to determine intestinal barrier and antioxidant functions of the host. , SC treatment increased the concentrations of glutathione and total antioxidant capacity, and expression of claudin-1 and claudin-3 in oxidation-damaged IPEC-J2 ( < 0.05). , SC treatment improved growth performance, intestinal morphology, expression of claudin-3, and activity of superoxide dismutase in mice ( < 0.05), but decreased interleukin-1β and interferon-γ concentrations in serum compared to the NC group ( < 0.05). Treatment with SC increased the populations of in the ileum and and in the colon, but decreased the abundances of and in the ileum and and in the colon compared with the NC group ( < 0.05). Concentrations of SCFA increased in the SC and PC groups than in the NC group ( < 0.05). Ileal protein expression of GPR 43 in the SC and PC groups was significantly greater than that in the NC group ( < 0.05). In conclusion, our findings confirmed the important role of sodium caprylate in improving intestinal barrier function and gut health by activating GPR 43 through regulating gut microbial metabolism.

摘要

短链脂肪酸(SCFA)是肠道微生物代谢产生的,据报道可通过激活 G 蛋白偶联受体(GPR)来调节宿主的免疫反应和肠道健康。目前尚不清楚中链脂肪酸(MCFA)是否通过激活 GPR 来改善肠道屏障功能。本研究旨在探讨辛酸钠(SC)和丁酸钠(PC)对 HO 处理的 IPEC-J2 及 C57/BL6 小鼠模型的抗氧化能力和肠道屏障功能的影响。在 和 试验中,用 SC 和 PC 处理氧化损伤的 IPEC-J2(NC)和小鼠,以确定宿主的肠道屏障和抗氧化功能。结果表明,SC 处理可提高氧化损伤的 IPEC-J2 ( < 0.05)中谷胱甘肽和总抗氧化能力的浓度,以及 Claudin-1 和 Claudin-3 的表达。此外,SC 处理可改善小鼠的生长性能、肠道形态、Claudin-3 的表达和超氧化物歧化酶的活性( < 0.05),但与 NC 组相比,血清中白细胞介素-1β和干扰素-γ的浓度降低( < 0.05)。与 NC 组相比,SC 处理可增加回肠中的 和 以及结肠中的 和 ,但减少回肠中的 和 以及结肠中的 和 ( < 0.05)。与 NC 组相比,SC 和 PC 组的 SCFA 浓度增加( < 0.05)。SC 和 PC 组的回肠 GPR43 蛋白表达明显高于 NC 组( < 0.05)。综上所述,本研究结果证实,辛酸钠通过调节肠道微生物代谢,激活 GPR43,在改善肠道屏障功能和肠道健康方面发挥重要作用。

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