[CAS NO. 80508-81-2]  Glaucocalyxin B

Glaucocalyxin A (GlnA) and (GlnB) dose-dependently decrease the growth of HL-60 cells with an IC ₅₀ of approximately 6.15 and 5.86 µM at 24 h, respectively. Both Gln A and B could induce apoptosis, G2/M-phase cycle arrest, DNA damage and the accumulation of reactive oxygen species (ROS) in HL-60 cells ^[1] . GlnB inhibits the proliferation of human cervical cancer cells in vitro through the induction of apoptosis andautophagy, which may be mediated by the phosphatidylinositol 4,5 bisphosphate 3 kinase/Akt signaling pathway. Treatment with GlnB inhibits the proliferation of HeLa and SiHa cervical cancer cell lines in a dose dependent manner. GlnB increases the apoptotic cell population of and enhanced poly (ADP ribose) polymerase 1 cleavage. GlnB also induces increased light chain 3 II/I protein cleavage, indicating the induction of autophagy. GlnB treatment increases the expression of phosphatase and tensin homolog and decreases the expression of phosphorylated protein kinase B ^[2] . Glaucocalyxin B (GLB), one of five ent-kauranoid diterpenoids, significantly decreased the generation of nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) in the lipopolysaccharide (LPS)-activated microglia cells ^[3] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.