본 연구는 150 mM HCl/60% 에탄올로 유도된 급성위염 동물 모델에서 치자 50% 에탄올 추출물(GFE)의 보호 효과를 평가하기 위해 수행되었다. 치자 추출물은 DPPH, ABTS 자유라디칼 소거능 실험을 통해 평가한 결과, 높은 항산화 활성을 나타냈다. GFE의 항위염 효과를 평가하기 위해 ICR 마우스를 이용하였고, Nor(정상군), Con(대조군), SC투여군(sucralfate 10 mg/kg 농도), GL투여군(치자 추출물 50 mg/kg 농도), GH투여군(치자 추출물 100 mg/kg 농도) 총 5군으로 나누어 실험을 진행하였다. 치자 추출물 투여 후위점막을 육안으로 관찰한 결과, 점막 손상을 현저히 감소시켰다. 위 조직에서 산화적 스트레스 바이오마커인 ROS와 ONOO-를 감소시켰다. 또한 위 조직을 western blot을 통해 분석한 결과, Nrf-2, HO-1, SOD, catalase 및 GPx-1/2 항산화 바이오마커들의 발현을 증가시켰으며, NF-κBp65, IκBα, COX-2, TNF-α 및 IL-1β 염증성 인자의 발현을 유의하게 억제하였다. 따라서 치자 50% 에탄올 추출물의 투여가 급성위염 동물실험 모델에서 위염 개선 효과가 있다고 사료된다.
This study examined the protective effects of gardenia fruit 50% ethanol extract (GFE) on a 150 mM HCl/60% ethanol-induced acute gastric injury model in mice. The antioxidant activities were evaluated through radical scavenging assays using 2,2-diphenyl-1-picrylhydrazyl and 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid). To evaluate the anti-gastritis effect of GFE, ICR mice were divided into 5 groups: Nor (normal group), Con (gastritis induced by HCl/ethanol with distilled water), SC treatment group (gastritis induced by HCl/ethanol treated with 10 mg/kg sucralfate), GL treatment group (gastritis induced by HCl/ethanol treated with 50 mg/kg GFE), and GH treatment group (gastritis induced by HCl/ethanol treated with 100 mg/kg GFE). The mice were pretreated with the extract (GL, GH) or drug (SC), and after 1 hour, 0.55 mL of 150 mM HCl/60% ethanol (v/v) mixture was administered orally. GFE improved the gastric lesions in a concentration-dependent manner. In addition, GFE inhibited the increased reactive oxygen species and ONOO<SUP>-</SUP> through the antioxidant pathway. The antioxidative biomarkers, including nuclear factor-erythroid 2-related factor 2, heme oxygenase-1, superoxide dismutase, catalase, and glutathione peroxidase-1/2, were increased significantly. In addition, the inflammatory related makers, nuclear factor-kappa B p65, inhibitor of nuclear factor kappa B alpha, cyclooxygenase-2, tumor necrosis factor-alpha, and interleukin-1 beta, were increased. GFE significantly inhibited inflammation through the antioxidant pathway. Therefore, GFE has potential for treating acute gastritis.