Background: Lung fibrosis is considered as an end stage for many lung diseases including lung inflammatory disease, autoimmune diseases and malignancy. There are limited therapeutic options with bad prognostic outcome. The aim of this study was to explore the effect of mesenchymal stem cells (MSCs) derived from bone marrow on Bleomycin (BLM) induced lung fibrosis in albino rats. Methods: 30 adult female albino rats were distributed randomly into 4 groups; negative control group, Bleomycin induced lung fibrosis group, lung fibrosis treated with bone marrow-MSCs (BM-MSCs) and lung fibrosis treated with cell free media. Lung fibrosis was induced with a single dose of intratracheal instillation of BLM. BM-MSCs or cell free media were injected intravenously 28 days after induction and rats were sacrificed after another 28 days for assessment. Minute respiratory volume (MRV), forced vital capacity (FVC) and forced expiratory volume 1 (FEV1) were recorded using spirometer (Power lab data acquisition system). Histological assessment was performed by light microscopic examination of H&E, and Masson’s trichrome stained sections and was further supported by morphometric studies. In addition, electron microscopic examination to assess ultra-structural changes was done. Confocal Laser microscopy and PCR were used as tools to ensure MSCs homing in the lung. Results: Induction of lung fibrosis was confirmed by histological examination, which revealed disorganized lung architecture, thickened inter-alveolar septa due excessive collagen deposition together with inflammatory cellular infiltration. Moreover, pneumocytes depicted variable degenerative changes. Reduction in MRV, FVC and FEV1 were recorded. BM-MSCs treatment showed marked structural improvement with minimal cellular infiltration and collagen deposition and hence restored lung architecture, together with lung functions. Conclusion: MSCs are promising potential therapy for lung fibrosis that could restore the normal structure and function of BLM induced lung fibrosis. Electronic supplementary material The online version of this article (10.1007/s13770-020-00294-0) contains supplementary material, which is available to authorized users.

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To evaluate the chondroprotective effect of L-carnitine in relation to glucosamine sulfate and in an experimental model of osteoarthritis (OA). Materials and methods: Thirty-two adult male Wister albino rats weighing 150-210 g were assigned randomly into 4 groups: 8 rats in each group, group I (control group), group II (MIA induced OA group), group III (MIA induced OA + glucosamine sulfate treated group), and group IV (MIA induced OA + L-carnitine treated group). Weight, knee diameter, and knee bend score were recorded on days 0, 1, 7, 14 and 28. On day 28 all animals were sacrificed. Synovial fluid of left knee was collected, and the interleukin-1b (IL-1b), Cartilage oligomeric matrix protein (COMP) and matrix metalloproteinase-13 (MMP-13) levels were measured by ELISA. The knee joints were removed and stained with H&E for histological evaluation. Results: The pathological abnormalities attributed to MIA induced arthritis was dramatically lowered in rats treated with glucosamine or L-carnitine. Synovial fluid levels of IL-1b, COMP and MMP-13 were increased in OA group, and significantly reduced with glucosamine or L-carnitine treated groups. Conclusion: L-Carnitine has a potential chondroprotective effect in this animal model of OA.

We compared the protective effects of melatonin and montelukast against cisplatin-induced testicular damage. Adult male rats were assigned to one of four groups: a control group, a cisplatin (Cis) group treated with a single intraperitoneal injection of 7 mg/kg cisplatin, a cisplatin + melatonin group (Cis-Mel) and a cisplatin + montelukast group (Cis-Mon) each treated with the same dose of cisplatin together with either oral melatonin (20 mg/kg) or oral montelukast (10 mg/kg) in 2 ml water from day 1 to day 10 starting on the day of the cisplatin injection. Cisplatin-induced oxidative stress, with a significant increase in testicular malonedialdehyde (MDA), decreased testicular glutathione (GSH), histological testicular damage and body weight loss. Additionally, increased abnormal sperm forms and decreased count and motility were noted. Melatonin and montelukast both rescued GSH concentrations, increased sperm count and motility and decreased abnormal forms. Montelukast resulted in better rescue of weight loss, while greater improvement in sperm count and testicular pathology, and a trend for decreased MDA were noted with melatonin. These findings suggest that melatonin and montelukast protect against different aspects of cisplatin-induced toxicity. Future studies should assess whether both drugs may have additive benefit when used in combination.

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ObjectivesStem cell therapy is a promising approach in the treatment of acute myocardial infarction (AMI). Mesenchymal stem cells (MSC) from bone marrow (BM-MSC) and adipose tissue (AT-MSC) are attractive and feasible for preclinical and clinical trials. In this study, we compared the therapeutic potential of BM-MSC and AT-MSC in repairing the hearts of rats with isoproterenol (ISO)-induced AMI.MethodsForty-two female rats were assigned into two groups; the optimization and the experimental group. The optimization groups were further subdivided into control group and the AMI induced group (using ISO). The experimental group was subdivided into AMI+cell-free media injected in the tail vein, AMI+BM-MSC, and AMI+AT-MSC groups treated with the intravenous injection of their respective cell types. Twenty-eight days after induction, electrocardiogram (ECG) was performed, and heart tissue samples were collected for histological assessment and cells tracing.ResultsMSC therapy repaired cardiac functions shown by the restoration of ST segment, QT and QRS intervals in the ECG when compared to the AMI group. Infarct area was significantly decreased, and cardiac tissue regeneration signs were shown on histopathological examination.ConclusionsBoth MSC sources proved to be equally efficient in the assessed parameters.

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