MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1016/j.intimp.2020.106680

Медицинская библиотека · International immunopharmacology · 2020

Luteolin alleviates myocardial ischemia reperfusion injury in rats via Siti1/NLRP3/NF-κB pathway.

Zhao Lingling, Zhou Zheng, Zhu Chunsheng, Fu Zhihui, Yu Dongsheng

СтатьяПеревод в очереди

Аннотация

The purpose of this study was to investigate the effects of luteolin (Lu) on myocardial ischemia-reperfusion (I/R) injury in rats. I/R model was established by ligating left anterior descending branch of coronary artery in rats. Cardiac hemodynamic measurement, myocardial infarction and damage assessment, antioxidant enzymes activities analysis, and various biochemical indexes of myocardial tissue were measured. Finally, the expression of proteins levels of Siti1/NLRP3/NF-κB pathway of myocardial tissue in rat were measured by Western Blotting. Lu obviously reduced the myocardial infarction in rats. Compared with sham group, I/R rats showed significant increase in LDH and CK-MB levels. In Lu group, LDH and CK-MB in I/R rats significantly decreased. In addition, Lu significantly reduced leukocyte infiltration compared with the sham group. On the other hand, Lu pretreatment effectively decreased the levels of cytokines in serum. The Siti1/NLRP3/NF-κBpathway in I/R group was significantly imbalance that in I/R group. Lu significantly restored the above protein changes. Lu may reduce I/R by regulation of Sirt1/NLRP3/NF-κBpathway.

Для цитирования: Zhao Lingling, Zhou Zheng, Zhu Chunsheng, Fu Zhihui, Yu Dongsheng. Luteolin alleviates myocardial ischemia reperfusion injury in rats via Siti1/NLRP3/NF-κB pathway.. International immunopharmacology. 2020. DOI: 10.1016/j.intimp.2020.106680.

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.