Kim Kyeong Jo, Kim Eun, Kang Wan Seok, Jeon Mijin, Choi Hakjoon, Lee Ki Hoon, Kim Mi-Hyeon, Kim Jin Seok, Na Chang-Su, Kim Sunoh
Central R&D Center, B&Tech Co., Ltd, Gwangju, Republic of Korea.
College of Korean Medicine, Dongshin University, Naju, Republic of Korea.
Dose Response. 2021 Oct 20;19(4):15593258211044329. doi: 10.1177/15593258211044329. eCollection 2021 Oct-Dec.
Previously, we demonstrated that the specific ratio of Korean multi-herbal formula (SR-5) exhibits hepatoprotective properties against ethanol-induced hepatic damage in rats. Chronic and excessive alcohol consumption is a major etiological factor involved in gastric disease and ulcer development induced by the inflammatory response and oxidative stress.
The present study evaluated the gastroprotective effects of SR-5 (100, 150, and 200 mg/kg) against hydrochloride acid/ethanol (HCl/EtOH)-induced and indomethacin/hydrochloride acid (INDO/HCl)-induced gastritis in a mouse model and the mechanisms involved.
All the tested doses of SR-5 significantly inhibited gastric lesions in the HCl/EtOH-induced ulcer model mice. Similarly, all the tested doses of SR-5 significantly inhibited gastric lesions in the INDO/HCl-induced ulcer model mice. Furthermore, mice pretreated with SR-5 had significantly increased gastric levels of enzymatic and nonenzymatic antioxidants, namely, catalase (CAT) and glutathione (GSH), with concomitant reductions in malondialdehyde (MDA) and reactive oxygen species (ROS) levels compared with those in the HCl/EtOH or INDO/HCl group. SR-5 suppressed the expression of nuclear factor-kappa B (NF-κB)/p65, inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and cyclooxygenase-2 (COX-2) to their normal values.
These findings are the first to demonstrate the powerful protective effect of SR-5 against gastric injury development and provide hope for clinical application.
此前,我们证明了韩国多草药配方(SR - 5)的特定比例对大鼠乙醇诱导的肝损伤具有肝保护作用。长期过量饮酒是由炎症反应和氧化应激引起的胃病和溃疡发展的主要病因。
本研究评估了SR - 5(100、150和200mg/kg)对小鼠模型中盐酸/乙醇(HCl/EtOH)诱导和吲哚美辛/盐酸(INDO/HCl)诱导的胃炎的胃保护作用及其相关机制。
所有测试剂量的SR - 5均显著抑制HCl/EtOH诱导的溃疡模型小鼠的胃损伤。同样,所有测试剂量的SR - 5均显著抑制INDO/HCl诱导的溃疡模型小鼠的胃损伤。此外,与HCl/EtOH或INDO/HCl组相比,用SR - 5预处理的小鼠胃中酶促和非酶促抗氧化剂(即过氧化氢酶(CAT)和谷胱甘肽(GSH))水平显著升高,同时丙二醛(MDA)和活性氧(ROS)水平降低。SR - 5将核因子-κB(NF-κB)/p65、诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)和环氧化酶-2(COX-2)的表达抑制至正常水平。
这些发现首次证明了SR - 5对胃损伤发展具有强大的保护作用,并为临床应用提供了希望。