Open veterinary journal · 2025
The equine placental extract ameliorates renal damage in mice with adenine-induced chronic kidney disease by inhibiting indoxyl sulfate production.
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.
Sugimoto Koji, Nakamura Junichi, Deng Dawei, Hirano Eiichi
Аннотация
BACKGROUND: Indoxyl sulfate (IS) is a dietary metabolite of tryptophan that is produced in the liver. It is a uremic toxin that facilitates the progression of chronic kidney disease (CKD). We previously observed that equine placental extract (ePE) inhibited IS synthesis in an in vitro inhibition assay using the liver S9 fraction.
AIM: This study was designed to investigate the effects of ePE on adenine-induced renal failure in mice at the histological and molecular levels to understand the mechanism of action of ePE.
METHODS: We assessed this effect through biochemical and histological in vivo analyses using a mouse model of CKD and an adenine diet, which induces renal damage through IS production.
RESULTS: ePE significantly suppressed serum, renal, and hepatic IS production in adenine diet-fed mice by inhibiting IS synthesis. Histological and semi-quantitative analyses using the tubulointerstitial injury index revealed that ePE effectively prevented the increase in adenine-induced mesangial-positive cell area. Additionally, ePE administration significantly suppressed adenine-induced renal fibrosis in mice. Moreover, immunohistochemical analysis demonstrated that ePE administration reduced the accumulation of F4/80-positive macrophages in the interstitial inflammatory infiltrates.
CONCLUSION: These results suggest that ePE ameliorates IS-associated renal injury in adenine diet-fed mice by reducing IS production in the interstitium of the kidneys.
AIM: This study was designed to investigate the effects of ePE on adenine-induced renal failure in mice at the histological and molecular levels to understand the mechanism of action of ePE.
METHODS: We assessed this effect through biochemical and histological in vivo analyses using a mouse model of CKD and an adenine diet, which induces renal damage through IS production.
RESULTS: ePE significantly suppressed serum, renal, and hepatic IS production in adenine diet-fed mice by inhibiting IS synthesis. Histological and semi-quantitative analyses using the tubulointerstitial injury index revealed that ePE effectively prevented the increase in adenine-induced mesangial-positive cell area. Additionally, ePE administration significantly suppressed adenine-induced renal fibrosis in mice. Moreover, immunohistochemical analysis demonstrated that ePE administration reduced the accumulation of F4/80-positive macrophages in the interstitial inflammatory infiltrates.
CONCLUSION: These results suggest that ePE ameliorates IS-associated renal injury in adenine diet-fed mice by reducing IS production in the interstitium of the kidneys.