EGCG Attenuates XXXX -Induced Inflammatory and Oxidative Stress Responses by Medicating the NOTCH Pathway.

@entity1 @entity32 @entity650 @entity310 @entity26 @entity3089 @entity125 @entity2842 @entity2071 @entity414
Background. The aim of this study is to investigate whether @entity3089 (EGCG) can prevent the UA-induced inflammatory effect of @entity1 umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro. Methods. HUVEC were subjected to @entity414 (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of @entity32 marker. The antioxidant activity was evaluated by measuring scavenged reactive @entity26 species (ROS). Functional studies of the role of @entity125 in HUVEC lines were performed using RNA interference analyses. Results. UA significantly increased the expressions of @entity650 , @entity2071 , @entity310 , and @entity2842 and the production of ROS in HUVEC. Meanwhile, the expression of @entity125 and its downstream effects significantly increased. Using siRNA, inhibition of @entity125 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of @entity125 showed that EGCG significantly decreased the expressions of inflammatory cytokines through @entity125 signaling pathways. Conclusions. In summary, our findings indicated that @entity125 plays an important role in the UA-induced inflammatory response, and the downregulation of @entity125 by EGCG could be an effective approach to decrease @entity32 and oxidative stress induced by UA.
