Purpose: To investigate the mechanism of polysaccharides from aloe vera (PAV), a main active ingredient of Aloe vera , treatment in pulpitis rats. Methods: Pulpitis were modeled by drilling the occlusal central fossa with Sprague Dawley rats. Next, the rats were treated with 20, 40, and 80 mg/kg PAV for three weeks, respectively. Computed tomography scanning assay, hematoxylin and eosin staining, and tartrate-resistant acid phosphatase staining were used to detect the pathology change. Then, levels of tumor necrosis factor-α, interleukin-1β, prostaglandin E 2 , and ciclooxigenase 2 were detected by enzyme-linked immunosorbent assay. The expressions of bone morphogenetic protein 2 human (BMP-2), osteocalcin, osterix, and runt-related transcription factor 2 (Runx2) were quantified by quantitative real-time polymerase chain reaction and Western blotting (WB). Finally, Wnt3a expression, p-GSK3β/GSK3β and p-β-catenin/β-catenin ratio were analyzed by WB. Results: PAV up regulated the bone mineral density, and reduced the breakage of the crown and cervical structures, and the necrosis of the crown and root pulp of pulpitis rats. In addition, results indicated that PAV could inhibit osteoblast formation. While osteoblasts’ number was decreased, proteins of BMP-2, osteocalcin, osterix, and Runx2 were up-regulated by PAV. Furthermore, PAV increased the Wnt3a expression and the p-β-catenin/β-catenin ratio, and decreased p-GSK3β/GSK3β ratio. Interestingly, these effects were all in dose dependence. Conclusions: PAV could inhibit pulp inflammation and promote osteoblasts differentiation via suppressing the activation of the Wnt/β-catenin signaling, enhancing the dental bone density.
This study assessed BMSC’s effect on melanoma cells. The melanoma A375 cells were assigned into blank group, BMSC group, ERK agonist group, AKT agonist group, ERK + AKT agonist group and ERK + AKT repressor group followed by analysis of VEGF expression, cell apoptotic rate, and the expression of MEK/ERK and PI3K/AKT signal proteins. ERK and AKT agonist group showed highest VEGF expression, lowest cell apoptosis and Bcl-2 and Bcl-2/Bax expression as well as highest MEK/ERK and PI3K/AKT signaling proteins followed by ERK agonist group and AKT agonist group. The apoptosis of melanoma cells could be prompted by BMSC which might be through restraining the activity of MEK/ERK and PI3K/AKT signal pathway. In conclusion, the apoptosis of melanoma cells is prompted by BMSC through restraining the activity of MEK/ERK and PI3K/AKT signal pathway, indicating that BMSC might be used as a novel approach for the treatment of melanoma.
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