MedElevator Войти в исследования
← Поиск публикаций

DOI 10.4314/ahs.v23i4.40

Медицинская библиотека · African health sciences · 2023

The immune-modulatory role of MSCs exerted by PI3K/AKT signaling pathway in kidney tissue after cyclophosphamide.

Eldien Heba M Saad, Alenzi Mohammed Jayed

СтатьяПеревод в очереди

Аннотация

BACKGROUND

Cyclophosphamide (CP) is one of the most effective immunosuppressive agents. To understand the mechanisms used by the CP and MSCs in the kidney, we investigated their effects on some pathways.

EXPERIMENTAL ANIMALS AND

METHODS

4 groups of female rats were used. GI: was the normal control group treated with saline solution. Groups G II, G III, and G IV were treated with CP. G I and G II groups were sacrificed on the fourth day after treatment., G III (Auto healing group) was left without treatment after the CP injection for six days. The G IV group was treated with MSCs on the fourth day after the CP injection. G III and G IV groups were sacrificed six days after treatment, and the kidney was removed and processed.

RESULTS

CP induced up-regulation in CD14 and CD21 positive cells and caspase. Significant down-regulation of previous markers in groups III and IV. CP exerted a downregulation effect on AKT/ PI3K, that were ameliorated in groups III and IV. A significant increase in P53, BCL2, as well as VEGF in Group IV (P < 0 05).

CONCLUSION

MSCs play a vital function in the immune inhibition in CP-treated rats through PI3K/AKT pathway.

Для цитирования: Eldien Heba M Saad, Alenzi Mohammed Jayed. The immune-modulatory role of MSCs exerted by PI3K/AKT signaling pathway in kidney tissue after cyclophosphamide.. African health sciences. 2023. DOI: 10.4314/ahs.v23i4.40.

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.