Inhibition of gene expression and production of iNOS and TNF-α in experimental model of neurodegenerative disorders stimulated microglia by Soy nano-isoflavone/stem cell-exosomes.

The present study evaluated the therapeutic potential of soybean nano-isoflavone extract versus bone marrow mesenchymal stem cells derived extracellular exosomes (BMSCs-EXs) in experimentally induced neurodegenerative diseases in rats (ND). In this study, 36 albino male rats were divided into four groups: Group I (control rats); Group II (induced neurodegenerative disease in rats by intraperitoneal injection of d-galactose (120 mg/kg/day for 2 months); Group III (ND-induced rats treated with nano-isoflavone in doses of 10 mg/kg by oral gavage for 3 months); and Group IV (ND-induced rats treated with a single dose injection of BMSCs-EXs. The effect of BMSCs-EXs was evaluated by cerebral oxidant/antioxidant biomarkers, and mRNA gene expression quantitation for cerebral tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (i-NOS) and GAPDH pathway-encoding genes by real time reverse transcription polymerase chain reaction (RT-PCR) techniques. Then, histopathological examination of the cerebral cortical tissues. Our results showed that BMSC-EXs were successfully isolated and characterized. d-galactose produced a significant rise in the number of damaged neurons, decreased cerebral superoxide dismutase and catalase activities, increased cerebral malondialdehyde levels, downregulated the cerebral TNF-α, and i-NOS pathway-encoding genes. Furthermore, BMSC-EXs and nano-isoflavone treatments repaired damaged cerebral tissue and recovered its function greatly following induction of neurodegenerative disease. Treatment with either MSCs-EXs or nano-isoflavones led to significant improvement in the histological findings, reversed the degenerative effect of d-galactose, and had a favorable therapeutic utility against d- galactose-induced neurodegenerative disease.

Extracellular vesicles derived from bone marrow mesenchymal stem cells repair functional and structural rat adrenal gland damage induced by fluoride.

The adrenal glands have striking morpho-biochemical features that render them vulnerable to the effects of toxins. AIMS: This study was conducted to explore the therapeutic utility of extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSC-EVs) against fluoride-induced adrenal toxicity. MATERIALS AND METHODS: The work included isolation and further identification of BMSC-EVs by transmission electron microscopy and flow cytometric analysis. Adrenal toxicity in rats was induced by oral administration of 300 ppm of sodium fluoride (NaF) in drinking water for 60 days followed by a single dose injection of BMSC-EVs. The effects of BMSC-EVs against NaF was evaluated by adrenal oxidant/antioxidant biomarkers, hormonal assay of plasma adrenocorticotrophic hormone (ACTH) and corticosterone (CORT) and mRNA gene expression quantitation for adrenal cortical steroidogenic pathway-encoding genes. Histopathological examination of the adrenal tissue was performed. KEY FINDINGS: BMSC-EVs were effectively isolated and characterized. NaF exposure decreased adrenal superoxide dismutase and catalase activities, increased adrenal malondialdehyde levels, elevated plasma ACTH, diminished CORT concentrations and downregulated the adrenal cortical steroidogenic pathway-encoding genes. In addition, NaF-induced marked adrenal histopathological lesions. SIGNIFICANCE: BMSC-EVs treatment repaired damaged adrenal tissue and recovered its function greatly following NaF consumption. BMSC-EVs reversed the toxic effects of NaF and reprogramed injured adrenal cells by activating regenerative processes.

Possible healing effects of Salvadora persica extract (MISWAK) and laser therapy in a rabbit model of a caustic-induced tongue ulcers: histological, immunohistochemical and biochemical study.

Caustic ingestion is a potentially detrimental event that can cause serious devastating damage on contact with tissues. Local exposure is associated with severe pain, swelling and ulceration. Caustics-induced oral ulcers can be painful enough to compromise the patient's quality of life. Treatment of oral ulcers is crucial in clinical practice. Albeit, some ulcers do not respond adequately to the conventional treatment. The current study was conducted to evaluate the potential healing effects of topical Salvadora persica (SP) extract, low-level laser (LLL) and high-level laser (HLL) therapies in a rabbit model of caustic-induced tongue ulcers and explore the underlying mechanisms. Fifty male rabbits with a caustic induced tongue ulcers were included in the study. Rabbits were equally divided into four groups: positive control (ulcer) group, SP, LLL and HLL groups in addition to the negative control (healthy) group. All treatments were given thrice weekly for 14 days. Results showed that acetic acid-induced tongue ulcers caused extensive structural tongue damage secondary to overexpression of apoptotic BAX, pathological angiogenesis indicated by VEGF overexpression, marked collagen fibers deposition as well as upregulation of tissue pro-inflammatory TNF-α and upregulation of tissue anti-inflammatory IL-10. The healing potential of topical SP, LLL and HLL therapy are mostly comparable. In conclusion, acetic acid-induced extensive tongue damage. Topical SP extract, LLL and HLL are equally effective therapies against caustics-induced tongue ulcers. However, we recommend SP extract, owing to its safety, non-invasiveness, availability and low cost.