MedElevator Войти в исследования
← Поиск публикаций

DOI 10.3967/bes2018.009

Медицинская библиотека · Biomedical and environmental sciences : BES · 2018

Serum Metabonomics of Articular Cartilage Destruction Induced by T-2 Toxin in Wistar Rats.

Zhu Lei, Zhao Zhi Jun, Ren Xiao Bin, Li Qiang, Ding Hua, Sun Zhou, Kao Qing Jun, Wang Li Hua

СтатьяПеревод в очереди

Аннотация

The molecular pathogenesis of T-2 toxin-induced cartilage destruction has not been fully unraveled yet. The aim of this study was to detect changes in serum metabolites in a rat anomaly model with articular cartilage destruction. Thirty healthy male Wistar rats were fed a diet containing T-2 toxin (300 ng/kg chow) for 3 months. Histopathological changes in femorotibial cartilage were characterized in terms of chondrocyte degeneration/necrosis and superficial cartilage defect, and the endogenous metabolite profile of serum was determined by UPLC/Q-TOF MS. Treated rats showed extensive areas of chondrocyte necrosis and superficial cartilage defect in the articular cartilage. In addition, 8 metabolites were found to change significantly in these rats compared to the control group, including lysoPE (18:0/0:0), lysoPC(14:0), lysoPC[18:4 (6Z,9Z,12Z,15Z)], lysoPC[(16:1(9Z)], lysoPC(16:0), L-valine, hippuric acid, and asparaginyl-glycine. These 8 metabolites associated with cartilage injury are mainly involved in phospholipid and amino acid metabolic pathways.

Для цитирования: Zhu Lei, Zhao Zhi Jun, Ren Xiao Bin, Li Qiang, Ding Hua, Sun Zhou, Kao Qing Jun, Wang Li Hua. Serum Metabonomics of Articular Cartilage Destruction Induced by T-2 Toxin in Wistar Rats.. Biomedical and environmental sciences : BES. 2018. DOI: 10.3967/bes2018.009.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

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.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.