miR-379-3p activates the MAPK/JNK/p38 pathway by negatively targeting DUSP1 expression to promote myocardial ischemia-reperfusion injury.

BackgroundMyocardial ischemia-reperfusion injury (MI/RI) is a primary cause of cardiomyocyte death in various cardiovascular diseases. MicroRNAs (miRNAs) play significant roles in MI/RI.ObjectiveThis study aims to elucidate the function and mechanism of miR-379-3p in this context.

Pristimerin suppresses colorectal cancer through inhibiting inflammatory responses and Wnt/β-catenin signaling.

Pristimerin, a triterpenoid, has exhibited potential anti-inflammatory and anti-tumor activities. Nevertheless, the role and mechanism of pristimerin in intestinal inflammation and colon cancer require further investigation. Here, we found that pristimerin protected mice from dextran sulfate sodium (DSS)-induced colitis, restoring epithelial damage and reducing tissue inflammation and inflammatory cell infiltration.

Pristimerin induces apoptosis and autophagy via activation of ROS/ASK1/JNK pathway in human breast cancer in vitro and in vivo.

Breast cancer is the most common malignant tumor in women, and progress toward long-term survival has stagnated. Pristimerin, a natural quinonemethide triterpenoid, exhibits potential anti-tumor effects on various cancers. However, the underlying mechanism remains poorly understood.

Pristimerin Induces Autophagy-Mediated Cell Death in K562 Cells through the ROS/JNK Signaling Pathway.

Chronic myeloid leukemia (CML) is a lethal malignancy, and the progress toward long-term survival has stagnated in recent decades. Pristimerin, a quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families, is well-known to exert potential anticancer activities. In this study, we investigated the effects and the mechanisms of action on CML.