Tubeimoside I is a naturally occuring triterpenoid saponin isolated from the medicinal herb B. paniculatum, with anti-inflammatory, apoptotic and antitumor activity.
Tubeimoside I is a naturally occuring triterpenoid saponin isolated from the medicinal herb B. paniculatum, with anti-inflammatory, apoptotic and antitumor activity. TBMS I inhibited the proliferation of both HepG2 and L-02 cells in a dose- and time-dependent manner, but HepG2 cells appeared more sensitive to the agent. When exposed to TBMS I for 24, 48 and 72 h, IC₅₀ for HepG2 cells versus L-02 cells were 15.5 vs. 23.1, 11.7 vs. 16.2, 9.2 vs. 13.1 (µM), respectively. TBMS I induced cell shrinkage, nuclear condensation and fragmentation, cell cycle arrest at the G2/M phase, mitochondrial membrane disruption, release of cytochrome c from the mitochondria, activation of caspase 3 and 9, and shifting Bax/Bcl-2 ratio from being anti-apoptotic to pro-apoptotic, all indicative of initiation and progression of apoptosis involving mitochondrial dysfunction[3]. TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI(Acute lung injury)[4]. Tubeimoside I attenuates osteoclastogenesis through down-regulating NF-κB signaling pathway, and is a potential candidate for the treatment of bone-destructive diseases like type 2 diabetic osteoporosis[5]. TBMS1 can effectively sensitize CDDP (Cisplatin) in CDDP-resistant human ovarian cancer cells through the down-regulation of the ERK1/2 and the up-regulation of the p38 signaling pathways[6]. TBMS1 might activate PTP1B(protein-tyrosine phosphatase 1B), which further hyperactivates MEK1/2-ERK1/2 cascade, thereby inhibiting cell proliferation in melanoma[7].
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