Chang Young Woon, Jang Jae Young, Kim Yong Ho, Kim Jung-Wook, Shim Jae-Jun
Departments of Internal Medicine, Kyung Hee University College of Medicine, Seoul, Korea.
Departments of Surgery, Kyung Hee University College of Medicine, Seoul, Korea.
Gut Liver. 2015 Jul;9(4):486-93. doi: 10.5009/gnl14040.
BACKGROUND/AIMS: The aims of this study were to investigate whether a broccoli sprout extract containing sulforaphane (BSES) inhibited the Helicobacter pylori infection density and exerted an antioxidative effect on gastric mucosal damage.
The enrolled subjects were randomized in a double-blinded manner into three groups. Finally, 33 H. pylori (+) BSES treatment subjects (group A), 28 H. pylori (+) placebo subjects (group B), and 28 H. pylori (-) BSES treatment subjects (group C) were studied. H. pylori infection density was indirectly quantified by a (13)C-urea breath test (UBT), and the ammonia concentration in gastric juice aspirates was measured through gastroscopic examination. Malondialdehyde (MDA), an oxidative damage biomarker, and reduced glutathione (GSH), an antioxidant biomarker, were measured in the gastric mucosa by an enzyme-linked immunosorbent assay.
BSES treatment did not significantly affect the UBT values or ammonia concentration in group A (p=0.634 and p=0.505, respectively). BSES treatment did significantly reduce mucosal MDA concentrations in group A (p<0.05) and group C (p<0.001), whereas the gastric mucosal GSH concentrations did not differ before and after treatment in any of the groups.
BSES did not inhibit the H. pylori infection density. However, BSES prevented lipid peroxidation in the gastric mucosa and may play a cytoprotective role in H. pylori-induced gastritis.
背景/目的：本研究旨在调查含有萝卜硫素的西兰花芽提取物（BSES）是否能抑制幽门螺杆菌感染密度，并对胃黏膜损伤发挥抗氧化作用。
将纳入的受试者以双盲方式随机分为三组。最终，对33名幽门螺杆菌阳性且接受BSES治疗的受试者（A组）、28名幽门螺杆菌阳性且接受安慰剂治疗的受试者（B组）和28名幽门螺杆菌阴性且接受BSES治疗的受试者（C组）进行了研究。通过碳-13尿素呼气试验（UBT）间接定量幽门螺杆菌感染密度，并通过胃镜检查测量胃液抽吸物中的氨浓度。采用酶联免疫吸附测定法在胃黏膜中测量氧化损伤生物标志物丙二醛（MDA）和抗氧化生物标志物还原型谷胱甘肽（GSH）。
BSES治疗对A组的UBT值或氨浓度无显著影响（分别为p = 0.634和p = 0.505）。BSES治疗显著降低了A组（p < 0.05）和C组（p < ０.001）的黏膜MDA浓度，而所有组治疗前后胃黏膜GSH浓度均无差异。
BSES未抑制幽门螺杆菌感染密度。然而，BSES可预防胃黏膜脂质过氧化，并可能在幽门螺杆菌诱导的胃炎中发挥细胞保护作用。
