Park Sang Woon, Oh Tae Young, Kim Yong Seok, Sim Hyejin, Park Sang Jong, Jang Eun Jung, Park Joo Sang, Baik Hyun Wook, Hahm Ki Baik
Digestive Disease Center and DMC-MECOX Biomedical Research Center, Jesaeng Hospital, Seongnam, Korea.
J Gastroenterol Hepatol. 2008 Jun;23(6):976-84. doi: 10.1111/j.1440-1746.2008.05333.x. Epub 2008 Apr 28.
Based on our previous studies that Artemisia asiatica extracts exert either antioxidative or cytoprotective actions against non-steroidal anti-inflammatory drugs or Helicobacter pylori-induced gastric mucosal injury, or imposes qualified ulcer healing in an acetic acid-induced gastric ulcer model, we investigated the protective effects of Artemisia asiatica extracts against ethanol-induced gastric mucosal injury.
Sprague-Dawley rats received 4 g/kg body weight (BW) of absolute ethanol intragastrically, which produced visible hemorrhagic gastric lesions 60 min later.
In this animal setting, the pretreatment of Artemisia extracts (30 or 100 mg/kg BW), 1 h before ethanol administration, significantly attenuated the source of gastric injury, which was assessed with gross and microscopic analysis (P < 0.01). Protection from alcohol-induced damage with Artemisia pretreatment was associated with significantly decreased lipid peroxidation, protecting gastric mucosa from glutathione depletion, as well as the inhibition of the cytochrome 2E1 ethanol-metabolizing enzyme. It attenuated the expressions of ethanol-induced pro-inflammatory cytokines, including interleukin (IL)-1beta and interferon-gamma, a weak activation of IL-10, the inhibition of the alcohol-induced overexpression of intercellular adhesion molecule-1, and the considerable induction of heat shock protein-72 expression in gastric mucosal homogenates.
The data suggest that the ethanol extracts of Artemisia asiatica exerted significant protection from alcohol-induced gastric mucosal injury through bio-regulation, which is essential for cytoprotection and anti-inflammation.
基于我们之前的研究,即亚洲艾提取物对非甾体抗炎药或幽门螺杆菌诱导的胃黏膜损伤具有抗氧化或细胞保护作用,或在醋酸诱导的胃溃疡模型中具有一定的溃疡愈合作用,我们研究了亚洲艾提取物对乙醇诱导的胃黏膜损伤的保护作用。
将4 g/kg体重的无水乙醇经胃内给予Sprague-Dawley大鼠,60分钟后可出现明显的出血性胃损伤。
在该动物模型中,在给予乙醇前1小时用亚洲艾提取物(30或100 mg/kg体重)预处理,可显著减轻胃损伤程度,通过大体和显微镜分析评估(P<0.01)。亚洲艾预处理对酒精诱导损伤的保护作用与脂质过氧化显著降低、保护胃黏膜免受谷胱甘肽耗竭以及抑制细胞色素2E1乙醇代谢酶有关。它减弱了乙醇诱导的促炎细胞因子的表达,包括白细胞介素(IL)-1β和干扰素-γ,轻度激活IL-10,抑制酒精诱导的细胞间黏附分子-1的过表达,并在胃黏膜匀浆中显著诱导热休克蛋白-72的表达。
数据表明,亚洲艾的乙醇提取物通过生物调节对酒精诱导的胃黏膜损伤发挥了显著的保护作用,这对细胞保护和抗炎至关重要。