School of Public Health, Guangdong Pharmaceutical University, Guangzhou, 510310, China.
School of Food Science, Guangdong Pharmaceutical University, Zhongshan, 528453, China.
Mol Nutr Food Res. 2023 May;67(10):e2200522. doi: 10.1002/mnfr.202200522. Epub 2023 Mar 28.
Gamma-aminobutyric acid (GABA) represents positive effects in stress model, but the exact antioxidant remains unclear. This study aims to determine what GABA do and how GABA interfere on oxidative stress in the small intestine of radiation-induced intestinal injury (RIII) mice.
C57BL/6J mice are gavaged. (1) Investigating the effects of GABA (50 100 mg kg BW d ) on basic information of healthy mice, and the survival time of RIII mice. (2) Evaluating the effect between GABA and theanine (100 mg kg BW d ) to RIII mice on the small intestine, by observing jejunum pathology, oxidative stress in small intestine and its mitochondria, and apoptosis protein expression. GABA reduces the weight loss and prolongs the median survival time of RIII mice. GABA and theanine reduce liver hyperemia, protect the villus crypt of jejunum, increase the antioxidant of duodenum and its mitochondria, to maintain the normal function and morphology. Besides, GABA increases B-cell lymphoma-2 (Bcl-2) expression and inhibits Caspase-3 activation, thereby inhibiting mitochondria-induced apoptosis.
GABA reduces the oxidative stress of small intestine in RIII mice, and maintains the normal morphology and function of mitochondria, which mechanism is that high Bcl-2 expression inhibits the autophagy of mitochondrial pathway, thus reducing intestinal barrier damage.
γ-氨基丁酸(GABA)在应激模型中表现出积极的影响,但确切的抗氧化作用尚不清楚。本研究旨在确定 GABA 的作用以及 GABA 如何干扰辐射诱导的肠损伤(RIII)小鼠小肠中的氧化应激。
C57BL/6J 小鼠灌胃。(1)研究 GABA(50、100mgkgBWd)对健康小鼠基本信息的影响,以及 RIII 小鼠的存活时间。(2)观察空肠病理、小肠及其线粒体氧化应激和凋亡蛋白表达,评估 GABA 与茶氨酸(100mgkgBWd)对 RIII 小鼠小肠的作用。GABA 减轻了 RIII 小鼠的体重减轻并延长了中位生存时间。GABA 和茶氨酸可减少肝脏充血,保护空肠绒毛隐窝,增加十二指肠及其线粒体的抗氧化能力,维持其正常功能和形态。此外,GABA 增加 B 细胞淋巴瘤-2(Bcl-2)的表达并抑制 Caspase-3 的激活,从而抑制线粒体诱导的细胞凋亡。
GABA 减轻了 RIII 小鼠小肠的氧化应激,维持了线粒体的正常形态和功能,其机制是高 Bcl-2 表达抑制线粒体途径的自噬,从而减少肠道屏障损伤。