Cepharanthine is an alkaloid derived from Stephania cepharantha Hayata, with possesses anti-inflammatory and antioxidative activities. CEP (Cepharanthine) dose-dependently inhibited the release of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 cells. Significantly, CEP dose-dependently suppressed NF-κB activation, IκBα degradation, and phosphorylation of ERK, JNK, and p38 induced by LPS. In vivo, it was also observed that CEP attenuated lung histopathologic changes and down-regulated the level of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, in the mouse acute lung injury model[3]. CEP inhibited Ca2+-induced swelling, depolarization, Cyt.c release, and the release of Ca2+ in a concentration dependent manner. CEP also inhibited Ca2+-induced generation of reactive oxygen species and Fe/ADP-induced swelling and lipid peroxidation. Furthermore, CEP suppressed Ca2+-induced thiol modification of adenine nucleotide transloase (ANT)[4]. Cepharanthine attenuates muscle and kidney injuries induced by limb ischemia/reperfusion (I/R)[5]. CEP attenuates cerebral I/R injury probably by inhibiting microglia activation and NLRP3 (NLR Family Pyrin Domain Containing 3) inflammasome-induced inflammation and reducing oxidative stress via suppressing 12/15-LOX signaling[6]. CEP could inhibit growth and motility of MCF-7 and MDA-MB-231 breast cancer cell[7].
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