Drug design, development and therapy · 2025
The Gastroprotective Effect of Hydrogen-Rich Coral Calcium in a Mouse Model of Peptic Ulcer Disease.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wu Hung-Tsung, Hsieh Ming-Tsung, Ou Horng-Yih, Chao Ting-Hsing, Tsai Liang-Miin
Аннотация
INTRODUCTION: Peptic ulcer disease (PUD), including gastric and duodenal ulcers, is primarily caused by Helicobacter pylori infection and non-steroid anti-inflammatory drugs, with additional contributors like stress, certain foods, and alcohol. Proton pump inhibitors (PPIs) are effective but with adverse effects, prompting the exploration of alternative therapies. Hydrogen-rich coral calcium (HRCC) is a novel antioxidative agent that exerted anti-oxidative and anti-inflammatory activities; however, the effects of HRCC on PUD were still obscure.
METHODS: The gastroprotective effects of HRCC were investigated in a mouse model of PUD, and macroscopic score was used to investigate the effects of HRCC on PUD. In addition, the expression of the pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), C-C motif chemokine ligand 2 (Ccl2), and interleukin-6 (IL-6) by real-time quantitative polymerase chain reaction. In addition, Western blots were used to evaluate the expressions of anti-oxidative enzymes, including catalase, glutathione peroxidase-1 (GPx), and superoxide dismutase (SOD).
RESULTS: HRCC attenuated ulcer severity induced by ethanol and hydrogen chloride ex vivo (n = 6). In addition, long-term treatment of HRCC for seven-day reduced ethanol and hydrogen chloride-induced ulcer formation (n = 6). Moreover, we found that HRCC treatment decreased immune cell infiltration, the gene expressions of pro-inflammatory cytokines (n = 6), and enhanced antioxidative enzyme levels (n = 3) in stomach of the animals in vivo.
CONCLUSION: HRCC has potential as a gastroprotective agent with anti-oxidative and anti-inflammatory activities, and its application may provide an alternative for treating PUD.
METHODS: The gastroprotective effects of HRCC were investigated in a mouse model of PUD, and macroscopic score was used to investigate the effects of HRCC on PUD. In addition, the expression of the pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), C-C motif chemokine ligand 2 (Ccl2), and interleukin-6 (IL-6) by real-time quantitative polymerase chain reaction. In addition, Western blots were used to evaluate the expressions of anti-oxidative enzymes, including catalase, glutathione peroxidase-1 (GPx), and superoxide dismutase (SOD).
RESULTS: HRCC attenuated ulcer severity induced by ethanol and hydrogen chloride ex vivo (n = 6). In addition, long-term treatment of HRCC for seven-day reduced ethanol and hydrogen chloride-induced ulcer formation (n = 6). Moreover, we found that HRCC treatment decreased immune cell infiltration, the gene expressions of pro-inflammatory cytokines (n = 6), and enhanced antioxidative enzyme levels (n = 3) in stomach of the animals in vivo.
CONCLUSION: HRCC has potential as a gastroprotective agent with anti-oxidative and anti-inflammatory activities, and its application may provide an alternative for treating PUD.