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Genistein plays an important role in the prevention of atherosclerosis. However, the underlying mechanisms have not been fully investigated. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (10, 100, and 1000 nM) for 6 h and then exposed to ox-LDL (50 mg/L) for another 24 h. Results showed that ox-LDL induced the expressions of E-selectin, P-selectin, monocyte chemotactic protein-1, interleukin-8, vascular adhesion molecule-1, and intercellular adhesion molecule-1, which were counteracted by genistein. The inhibitory effect was further enhanced with the augment of genistein (10, 100, and 1000 nM). Further analyses demonstrated the effect of genistein was associated with reducing miR-155 and elevating SOCS1, and miR-155 mimics or SOCS1 siRNA acted similarly in genistein ameliorating inflammation. Moreover, the effect of genistein was accompanied with the inhibition of the NF-ĸB signaling pathway. The present study indicates that genistein could reverse ox-LDL-induced inflammation through miR-155/SOCS1-mediated repression of the NF-ĸB signaling pathway in HUVECs.

Obesity is a chronic health condition characterized by the accumulation of excessive body fat which can lead to and exacerbate cardiovascular disease, type‐II diabetes, high blood pressure, and cancer through systemic inflammation. Unfortunately, visualizing key mediators of the inflammatory response, such as monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH), in a selective manner is a profound challenge owing to an overlapping substrate scope that involves arachidonic acid (AA). Specifically, these enzymes work in concert to generate AA, which in the context of obesity, has been implicated to control appetite and energy metabolism. In this study, we developed the first selective activity‐based sensing probes to detect MGL (PA‐HD‐MGL) and FAAH (PA‐HD‐FAAH) activity via photoacoustic imaging. Activation of PA‐HD‐MGL and PA‐HD‐FAAH by their target enzymes resulted in 1.74‐fold and 1.59‐fold signal enhancements, respectively. Due to their exceptional selectivity profiles and deep‐tissue photoacoustic imaging capabilities, these probes were employed to measure MGL and FAAH activity in a murine model of obesity. Contrary to conflicting reports suggesting levels of MGL can be attenuated or elevated, our results support the latter. Indeed, we discovered a marked increase of both targets in the gastrointestinal tract. These key findings set the stage to uncover the role of the endocannabinoid pathway in obesity‐mediated inflammation. [ABSTRACT FROM AUTHOR]