Emodin attenuates apoptosis and inflammation induced by LPS through up-regulating lncRNA TUG1 in murine chondrogenic ATDC5 cells

Conclusion Emodin mitigated the LPS-induced apoptosis and inflammation in ATDC5 cells. Emodin might function through inhibiting the Notch and NF-κB pathways via up-regulating TUG1. Our findings might furnish a prospective therapeutic strategy using emodin for OA. Graphical abstract
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research