Fraxinellone, a natural product isolated and purified from the root barks of Dictamnus dasycarpus Turcz. with neuroprotective, vasorelaxing, insecticidal, and antimicrobial activities, is a selective blocker of voltage-dependent Ca2+ channel, while dictamine relaxed the rat aorta by suppressing the Ca2+ influx through both voltage-dependent and receptor-operated Ca2+ channels, and can dramatically induce apoptosis of activated peripheral CD4(+) T cells in vivo, consequently resulting in less CD4(+) T-cell activation and infiltration to the liver.
Fraxinellone is a natural product isolated from the D. dasycarpus plant, which has been shown to exhibit neuroprotective and anti-inflammatory activities. Fraxinellone, in a dose-dependented manner, inhibited the expression of programmed cell death ligand-1 (PD-L1), which plays a pivotal role in tumorigenesis[3]. Fraxinellone attenuated the clinical and histologic features of inflammatory arthritis in CIA (collagen-induced arthritis) mice. Fraxinellone alleviated synovial inflammation and osteoclastogenesis in mice[4]. Intraperitoneal injection of fraxinellone significantly inhibited the pancreatic activation of multiple inflammasome molecules such as NACHT, LRR and PYD domains-containing protein 3 (NLRP3), PY-CARD, caspase-1, IL-18, and IL-1β during AP. In addition, fraxinellone treatment inhibited pancreatic injury, elevation in serum amylase and lipase activities, and infiltration of inflammatory cells such as neutrophils and macrophages but had no effect on pancreatic edema[5]. Moreover, fraxinellone administration caused growth arrest and certainly repressed the activity of senescence associated β-galactosidase as well as the expression of senescence-associated-genes[6].
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