Regenerative therapy · 2026
Menstrual blood-derived stromal cells exhibit superior protection against lung injury in myocardial Infarction-Induced heart failure in rats compared to bone marrow-derived stromal cells.
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.
Manshori Mahmood, Saffarian Zahra, Aboutaleb Nahid, Golshahi Hannaneh
Аннотация
INTRODUCTION: Lung injury is a frequent complication following heart failure (HF) due to systemic inflammation, hypoxia, and reduced cardiac function. This study compared the therapeutic effects of menstrual blood-derived stromal cells (MenSCs) and bone marrow-derived stromal cells (BMSCs) on HF-induced lung injury in rats.
METHODS: Twenty male Wistar rats underwent permanent ligation of the left anterior descending coronary artery to induce myocardial infarction (MI). They were randomly assigned to receive intravenous injections of MenSCs (2 × 106 cells), BMSCs (2 × 106 cells), or PBS 7 days post-MI. Cardiac function was assessed by echocardiography, and lung tissues were analyzed 28 days post-cell administration. Histopathology (H&E and Masson's trichrome staining) evaluated pulmonary structural changes and fibrosis, TUNEL assay assessed apoptosis, and immunohistochemistry measured NF-κB and iNOS expression.
RESULTS: Results showed that MenSC treatment significantly improved left ventricular ejection fraction compared with MI and BMSC groups (both P < 0.0001). MenSCs markedly reduced pulmonary injury scores and apoptotic cell numbers compared with both untreated and BMSC-treated rats (P < 0.0001). Both cell types reduced pulmonary fibrosis compared to MI (P < 0.0001). Both MenSCs and BMSCs similarly reduced NF-κB expression, whereas only MenSCs effectively decreased iNOS expression (P < 0.0001). Human mitochondrial antibody staining confirmed successful homing of both cell types to injured lung tissue.
CONCLUSION: systemic administration of MenSCs effectively ameliorated HF-induced lung injury through anti-inflammatory, anti-apoptotic, and anti-fibrotic mechanisms. Compared with BMSCs, MenSCs demonstrated superior therapeutic potential, highlighting their promise as a non-invasive and immunologically favorable cell source for regenerative therapy in remote organ injury following MI.
METHODS: Twenty male Wistar rats underwent permanent ligation of the left anterior descending coronary artery to induce myocardial infarction (MI). They were randomly assigned to receive intravenous injections of MenSCs (2 × 106 cells), BMSCs (2 × 106 cells), or PBS 7 days post-MI. Cardiac function was assessed by echocardiography, and lung tissues were analyzed 28 days post-cell administration. Histopathology (H&E and Masson's trichrome staining) evaluated pulmonary structural changes and fibrosis, TUNEL assay assessed apoptosis, and immunohistochemistry measured NF-κB and iNOS expression.
RESULTS: Results showed that MenSC treatment significantly improved left ventricular ejection fraction compared with MI and BMSC groups (both P < 0.0001). MenSCs markedly reduced pulmonary injury scores and apoptotic cell numbers compared with both untreated and BMSC-treated rats (P < 0.0001). Both cell types reduced pulmonary fibrosis compared to MI (P < 0.0001). Both MenSCs and BMSCs similarly reduced NF-κB expression, whereas only MenSCs effectively decreased iNOS expression (P < 0.0001). Human mitochondrial antibody staining confirmed successful homing of both cell types to injured lung tissue.
CONCLUSION: systemic administration of MenSCs effectively ameliorated HF-induced lung injury through anti-inflammatory, anti-apoptotic, and anti-fibrotic mechanisms. Compared with BMSCs, MenSCs demonstrated superior therapeutic potential, highlighting their promise as a non-invasive and immunologically favorable cell source for regenerative therapy in remote organ injury following MI.