Light-curing adhesive and oxalate-type desensitizing agents exhibited better reduction of dentinal fluid flow rate than did protein-precipitation and fluoride-type desensitizing agents based on measurements by a new fluid flow measuring device of subnanoliter scale. SUMMARYThe aims of this study were to examine changes in dentinal fluid flow (DFF) during the application of a desensitizing agent and to compare the permeability reduction levels among different types of desensitizing agents.A cervical cavity was prepared for the exposure of cervical dentin on an extracted human premolar connected to a subnanoliter fluid flow measuring device under 20 cm of water pressure. The cavity was acid-etched with 32% phosphoric acid to make dentin highly permeable. The different types of desensitizing agents that were applied on the cavity were Seal&Protect as the light-curing adhesive type, SuperSeal and BisBlock as oxalate types,
Background: Oxidative radicals are major environmental causes of human skin damage. Oxidative defense factors, including nuclear factor erythroid-derived 2-related factor 2 (Nrf2), are centrally involved in repairing skin cells or protecting them from oxidative damage. Coriandrum sativum L. (coriander; CS) is a commonly consumed food and a traditional phytomedicine in Asia and Europe. In this study, we examined the protective effects of a standardized CS leaf extract against oxidative stress in human HaCaT keratinocytes. Methods and Results: CS significantly and dose-dependently protected cells against reduced cell viability caused by H2O2-induced damage, as assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Other assays demonstrated that CS protected HaCaT cells by increasing the levels of glutathione and activities of oxidative defense enzymes, such as superoxide dismutase and catalase. Moreover, it increased the expression of activated Nrf2, which plays a crucial role in protecting skin cells against oxidative stress. Conclusion: These results suggest that CS protects human keratinocytes from H2O2-induced oxidative stress through antioxidant effects.
Background and purpose: Apoptosis is a fundamental process required for neuronal development but also occurs in most of the common neurodegenerative disorders. In an attempt to obtain an anti-apoptotic neuroprotective compound from natural products, we isolated the diterpenoids, pinusolide and 15-MPA, from B. orientalis and investigated their neuroprotective activity against staurosporine (STS) -induced neuronal apoptosis. In addition, we determined the anti-apoptotic mechanism of these compounds in rat cortical cells. Experimental approach: Primary cultures of rat cortical cells injured by STS were used as an in vitro assay system. Cells were pretreated with pinusolide or 15-MPA before exposure to STS. Anti-apoptotic activities were evaluated by the measurement of cytoplasmic condensation and nuclear fragmentation. The levels of cellular peroxide, malondialdehyde (MDA) and [Ca 2 þ ] i , as well as the activities of superoxide dismutase (SOD) and caspase-3/7, were measured. Key results: Pinusolide and 15-MPA, at a concentration of 5.0 ìM, reduced the condensed nuclei and rise in [Ca 2 þ ] i that accompanies apoptosis induced by 100 nM STS. Pinusolide and 15-MPA also protected the cellular activity of SOD, an antioxidative enzyme reduced by STS insult. Furthermore, the overproduction of reactive oxygen species and lipid peroxidation induced by STS was significantly reduced in pinusolide and 15-MPA treated cells. In addition, pinusolide and 15-MPA inhibited STS-induced caspase-3/7 activation. Conclusions and Implications: These results show that pinusolide and 15-MPA protect neuronal cells from STS-induced apoptosis, probably by preventing the increase in [Ca 2 þ ] i and cellular oxidation caused by STS, and indicate that they could be used to treat neurodegenerative diseases.
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