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Sanguinarine is an alkaloid obtained from the bloodroot plant Sanguinaria canadensis and has beneficial effects on oxidative stress and inflammatory disorders. Previous reports have demonstrated that sanguinarine also exhibit anticancer properties. In the current study, we investigated the effects of sanguinarine on HT-29 human colon cancer cells. It was observed that sanguinarine treatment induces a dose-dependent increase in apoptosis of human colon cancer cells. We also investigated the effects of sanguinarine on the expression of apoptosis-associated proteins, and the results revealed that there was an increase in Bax and a decrease in B-cell lymphoma 2 (Bcl-2) protein levels. Moreover, sanguinarine treatment significantly increases the activation of caspases 3 and 9 that are the key executioners in apoptosis. Our results suggest that sanguinarine induces apoptosis of HT-29 human colon cancer cells and may have a potential therapeutic use in the treatment of human colon cancer.

Three dimensional tissue engineered scaffolds for the treatment of critical defect have been usually fabricated by salt leaching or gas forming technique. However, it is not easy for cells to penetrate the scaffolds due to the poor interconnectivity of pores. To overcome these current limitations we utilized a rapid prototyping (RP) technique for fabricating tissue engineered scaffolds to treat critical defects. The RP technique resulted in the uniform distribution and systematic connection of pores, which enabled cells to penetrate the scaffold. Two kinds of materials were used. They were poly(ε-caprolactone) (PCL) and poly(D, L-lactic-glycolic acid) (PLGA), where PCL is known to have longer degradation time than PLGA. In vitro tests supported the biocompatibility of the scaffolds. A 12-week animal study involving various examinations of rabbit tibias such as micro-CT and staining showed that both PCL and PLGA resulted in successful bone regeneration. As expected, PLGA degraded faster than PCL, and consequently the tissues generated in the PLGA group were less dense than those in the PCL group. We concluded that slower degradation is preferable in bone tissue engineering, especially when treating critical defects, as mechanical support is needed until full regeneration has occurred.

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Background/AimsThe aim of this study was to determine whether the routine closure of mucosal defects after endoscopic submucosal dissection (ESD) can enhance mucosal healing and reduce ESD-associated bleeding.MethodsPatients with gastric epithelial neoplasias and no obvious submucosal invasion were prospectively enrolled. Mucosal defects were left untreated in the control group. In the study group, mucosal closure was attempted with a 2-channel endoscope, a detachable snare, and clips. All participants received a second-look endoscopy the day after ESD, and coagulation therapy was administered to patients with visible vessels and active bleeding points.ResultsFifty-two patients were enrolled in the study, and 26 patients were assigned to each group. Complete mucosal defect closure occurred in 16 patients (61%) in the study group; incomplete closure occurred in 8 patients (31%) in the study group, and failed closure occurred in 2 patients (8%). Coagulation therapy at the second-look endoscopy was performed more often in the control group than in the study group (31% vs 4%, p=0.024). There were no significant differences in the incidence of immediate or delayed bleeding or in the two-week decrease in hemoglobin between the groups. The prevalence of open ulcers after 8 weeks was significantly lower in the study group than in the control group (18% vs 43%, p=0.012).ConclusionsRoutine mucosal closure after ESD supports earlier healing of artificial ulcers. A larger-scale trial is necessary to determine whether mucosal closure can reduce ESD-associated bleeding.

The use of light for medical treatment has been studied previously. In this study, we examined the effect of light from a red light-emitting diode on osteogenic differentiation of mouse mesenchymal stem cells (D1 cells) which were cultured in the presence of osteogenic differentiation medium (ODM) for 3 days, then exposed to a red light-emitting diode (LED) light of 647 nm wavelength once for 10 s, 30 s or 90 s with radiation energies of 0.093 J, 0.279 J and 0.836 J, respectively. D1 cells in the presence of ODM differentiated into osteoblasts, and this process was enhanced on exposure to LED light in ODM medium. This effect was confirmed by increased Alizarin red staining, higher alkaline phosphatase (ALP) activity, higher mRNA expressions of osteocalcin, collagen type I, osteopontin and Runt-related transcription factor2 (Runx2), and higher levels by reverse transcriptase-polymerase chain reaction (RT-PCR) and by increased immunofluorescence staining against cluster of differentiation 44 (CD44) by immunofluorescence microscopy, confocal microscopy and flow cytometric analysis. These data suggest that osteogenic differentiation of mesenchymal stem cells (MSCs) in ODM is enhanced by LED light exposure.