Kubota Atsuhito, Kobayashi Masaki, Sarashina Sota, Takeno Reiko, Yasuda Genki, Narumi Katsuya, Furugen Ayako, Takahashi-Suzuki Natsuko, Iseki Ken
Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University.
Department of Pharmacy, Hokkaido University Hospital.
Biol Pharm Bull. 2018;41(12):1874-1878. doi: 10.1248/bpb.b18-00338.
The aims of this study were to determine the effects of gamma-aminobutyric acid (GABA) on immunoglobulin A (IgA) secretion from Peyer's patch (PP) cells; to assess rat alpha-defensin-5 (RD-5) expression in the rat small intestine; and to determine the effect of GABA on intestinal ischemia reperfusion (I/R) injury-induced intestinal innate immunity. We found that GABA caused an increase in IgA secretion in the presence and absence of lipopolysaccharide (LPS). Moreover, GABA also significantly increased the mRNA levels of RD-5 and superoxide dismutase (Sod) 1, 3. Intestinal I/R was induced by a 30-min occlusion of the superior mesenteric artery followed by a reperfusion for 60-min. This led to a significant decrease in IgA secretion, and mRNA levels of RD-5 and Sod 1-3 in the ileum. On the other hand, administration of GABA before I/R induction had a significant protective effect against oxidative injury and attenuated the effects on intestinal immunity.
本研究的目的是确定γ-氨基丁酸(GABA)对派尔集合淋巴结(PP)细胞分泌免疫球蛋白A(IgA)的影响;评估大鼠α-防御素-5(RD-5)在大鼠小肠中的表达;并确定GABA对肠缺血再灌注(I/R)损伤诱导的肠道天然免疫的影响。我们发现,无论有无脂多糖(LPS),GABA都会导致IgA分泌增加。此外,GABA还显著提高了RD-5和超氧化物歧化酶(Sod)1、3的mRNA水平。通过肠系膜上动脉闭塞30分钟,然后再灌注60分钟来诱导肠I/R。这导致回肠中IgA分泌以及RD-5和Sod 1-3的mRNA水平显著降低。另一方面,在诱导I/R之前给予GABA对氧化损伤具有显著的保护作用,并减弱了对肠道免疫的影响。