Traditional kombucha is a fermented black tea extract and sugar. Sweetened black tea (10% w/v) and wheatgrass juice (WGJ) were mixed in various ratios and used as fermentation substrate for enhancing phenolic compounds and antioxidant activity. Starter, comprising of yeast (Dekkera bruxellensis) and acetic acid bacteria (Gluconacetobacter rhaeticus and Gluconobacter roseus), was inoculated at 20% (v/v), and fermented statically at 29 ± 1°C for 12 days. The results showed that the total phenolic and flavonoid contents and antioxidant activity of the modified kombucha were higher than those of traditional preparations. All WGJ-blended kombucha preparations were characterized as having higher concentrations of various phenolic compounds such as gallic acid, catechin, caffeic acid, ferulic acid, rutin, and chlorogenic acid as compared to traditional ones. Addition of WGJ resulted in the 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging ability of kombucha being > 90%, while the oxygen radical absorbance capacity increased from 5.0 μmol trolox equivalents/mL to 12.8 μmol trolox equivalents/mL as the ratio of WGJ increased from 0% to 67% (v/v). The highest antioxidant activity was obtained using a 1:1 (v/v) black tea decoction to WGJ ratio and 3 days of fermentation, producing various types of phenolic acids. These results suggest that intake of fermented black tea enhanced with wheatgrass juice is advantageous over traditional kombucha formulas in terms of providing various complementary phenolics and might have more potential to reduce oxidative stress.
Camphorquinone (CQ) is a popularly-used photosensitizer in composite resin restoration. In this study, the effects of CQ on cytotoxicity and inflammation-related genes and proteins expression of pulp cells were investigated. The role of reactive oxygen species (ROS), ATM/Chk2/p53 and hemeoxygenase-1 (HO-1) and MEK/ERK signaling was also evaluated. We found that ROS and free radicals may play important role in CQ toxicity. CQ (1 and 2 mM) decreased the viability of pulp cells to about 70% and 50% of control, respectively. CQ also induced G2/M cell cycle arrest and apoptosis of pulp cells. The expression of type I collagen, cdc2, cyclin B, and cdc25C was inhibited, while p21, HO-1 and cyclooxygenase-2 (COX-2) were stimulated by CQ. CQ also activated ATM, Chk2, and p53 phosphorylation and GADD45α expression. Besides, exposure to CQ increased cellular ROS level and 8-isoprostane production. CQ also stimulated COX-2 expression and PGE2 production of pulp cells. The reduction of cell viability caused by CQ can be attenuated by N-acetyl-L-cysteine (NAC), catalase and superoxide dismutase (SOD), but can be promoted by Zinc protoporphyin (ZnPP). CQ stimulated ERK1/2 phosphorylation, and U0126 prevented the CQ-induced COX-2 expression and prostaglandin E2 (PGE2) production. These results indicate that CQ may cause cytotoxicity, cell cycle arrest, apoptosis, and PGE2 production of pulp cells. These events could be due to stimulation of ROS and 8-isoprostane production, ATM/Chk2/p53 signaling, HO-1, COX-2 and p21 expression, as well as the inhibition of cdc2, cdc25C and cyclin B1. These results are important for understanding the role of ROS in pathogenesis of pulp necrosis and pulpal inflammation after clinical composite resin filling.
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