Suppression of the inflammation and fibrosis in Asherman syndrome rat model by mesenchymal stem cells: histological and immunohistochemical studies.

INTRODUCTION: Asherman syndrome (AS) is a symptomatic intrauterine adhesion caused by endometrial basal layer fibrosis as a result of either uterine cavity surgery or infection leading to many complications. There is a concern to repair the injured tissues by using bone marrow mesenchymal stem cells (BM-MSCs). We aimed in this study to develop an animal model of AS and evaluate the anti-inflammatory and anti-fibrotic effects of BM-MSCs in this model through histological, immunohistochemical, and morphometric studies. MATERIAL AND METHODS: Forty-two adult female adult albino rats were divided into (i) donor group composed of 2 rats used for isolation and propagation of BM-MSCs, and (ii) experimental groups: 40 rats equally divided into 4 groups: GpI (control), GpII (AS model), GpIII (BM-MSCs-treated AS rats), GpIV (untreated AS rats). Histological staining and immunohistochemical (IHC) detection of proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), and nuclear factor-kappa beta (NF-kB) were performed. The results were evaluated by morphometric and statistical analysis. RESULTS: Significant endometrial thinning, fibrosis, and degeneration of the endometrial epithelium with a significant decrease in PCNA and VEGF immunoexpression and a significant increase in NF-kB immunoexpression were detected in GpII and GpIV groups. These changes were substantially reversed in BM-MSCs-treated animals. CONCLUSIONS: BM-MSCs treatment resulted in substantial improvement of intrauterine adhesion in the rat model of Asherman syndrome.

Histological Study on the Protective Effect of Endogenous Stem Cell Mobilization in Busulfan-Induced Testicular Injury in Albino Rats.

BACKGROUND: Testicular damage is one of the most hazardous effects of chemotherapy as it is frequently associated with oligozoospermia and azoospermia. AIM OF THE WORK: This study aimed at evaluating the protective effect of hematopoietic stem cell mobilization by granulocyte colony-stimulating factor (G-CSF) in a rat model of busulfan-induced testicular injury. MATERIALS AND METHODS: Twenty-four adult albino rats were divided into four groups: group I, the control, Group II: rats received two doses of busulfan (each 15 mg/kg) intraperitoneally (IP) with 14 days interval, Group III: rats received busulfan and left untreated, and Group IV received busulfan IP then G-CSF (70 µg/kg/day) subcutaneously for 5 consecutive days. Testicular sections were stained with H and E and immunohistochemically for CD34, proliferating cell nuclear antigen (PCNA) and caspase-3, and semithin sections were stained with toluidine blue. RESULTS: Groups II and III showed loss of the normal histological architecture of the testis and spermatogenic cells, with increased apoptosis confirmed by significantly increased caspase-3 and significantly decreased PCNA immunoexpression. While Group IV revealed improved testicular histology, decreased apoptosis, and increased proliferative capacity of spermatogenic cells. This was confirmed by significantly decreased caspase-3 immunoexpression and increased PCNA immunoreaction. CONCLUSION: Mobilization of stem cells with G-CSF was found to improve the testicular histology following busulfan chemotherapy in albino rats.