Anemarsaponin B
Anemarsaponin B can inhibit PAF-induced rabbit platelet aggregation in vitro. Anemarsaponin B has anti-inflammatory effect in LPS-treated RAW 264.7macrophages, the effect is associated with the inhibition of NF-κB transcriptional activity, possibly via the p38 MAP kinase pathway.
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Yao Xue Xue Bao. 1992;27(1):26-32.
[Studies on the active constituents of Anemarrhena asphodeloides bunge].[Pubmed:
1529709]
METHODS AND RESULTS:
From the ethanol extract of the Anemarrhena asphodeloides Buge (Liliaceae), a new steroidal suponin Anemarsaponin B and two known saponins anemarsaponin A1 and A2 were isolated. On the basis of chemical evidences and spectral analysis (UV, IR, EI-MS, FAB-MS, 1H-NMR and 13C-NMR), the structure of Anemarsaponin B was elucidated as 26-O-beta-D-glucopyranosylfurost-20(22)-ene-3 beta,26-diol-3-O-beta-D- glucopyranosyl(1----2)-beta-D-galactopyranoside.
CONCLUSIONS:
Preliminary pharmacological tests showed that Anemarsaponin B could inhibit PAF-induced rabbit platelet aggregation in vitro.
Planta Med. 1991 Oct;57(5):460-2.
A new active steroidal saponin from Anemarrhena asphodeloides.[Pubmed:
1798801]
METHODS AND RESULTS:
A new active steroidal saponin, Anemarsaponin B, was isolated from the rhizomes of Anemarrhina asphodeloides. The structure of Anemarsaponin B was elucidated as 26-O-beta-D-glucopyranosylfurost-20(22)-ene-3 beta, 26-diol-3-O-beta-D-glucopyranosyl-(1----2)-beta-D-galactopyranoside by chemical and spectral studies.
CONCLUSIONS:
Preliminary pharmacological tests showed that Anemarsaponin B could inhibit PAF-induced rabbit platelet aggregation in vitro.
Food Chem Toxicol . 2009 Jul;47(7):1610-7.
Anti-inflammatory effect of anemarsaponin B isolated from the rhizomes of Anemarrhena asphodeloides in LPS-induced RAW 264.7 macrophages is mediated by negative regulation of the nuclear factor-kappaB and p38 pathways[Pubmed:
19375480]
Abstract
Anemarrhena asphodeloides is widely used in traditional Chinese medicine, and is known to have anti-diabetic and diuretic effects. In this study, we evaluated the anti-inflammatory effects of Anemarsaponin B (ASB), a steroidal saponin isolated from the rhizomes of A. asphodeloides (Liliaceae), in LPS-stimulated RAW 264.7 macrophage cell line. ASB significantly and dose-dependently decreased the protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). ASB also reduced the expressions and productions of pro-inflammatory cytokines, including those of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Electrophoretic mobility shift assay (EMSA) and reporter gene assays revealed that ASB attenuated the LPS-induced DNA binding and transcriptional activity of nuclear factor-kappa B (NF-kappaB). In addition, it was found that pretreatment with ASB significantly inhibited the nuclear translocation of the p65 subunit of NF-kappaB by blocking the phosphorylation of inhibitory kappa B-alpha (IkappaB-alpha). On the other hand, ASB inhibited the phosphorylation of MAP kinase kinases 3/6 (MKK3/6) and mixed lineage kinase 3 (MLK3), which are both involved in the p38 pathway. Taken together, these results suggest that anti-inflammatory effect of ASB in LPS-treated RAW 264.7 macrophages is associated with the inhibition of NF-kappaB transcriptional activity, possibly via the p38 MAP kinase pathway.
Food Chem Toxicol. 2009 Jul;47(7):1610-7.
Anti-inflammatory effect of anemarsaponin B isolated from the rhizomes of Anemarrhena asphodeloides in LPS-induced RAW 264.7 macrophages is mediated by negative regulation of the nuclear factor-kappaB and p38 pathways.[Pubmed:
19375480]
Anemarrhena asphodeloides is widely used in traditional Chinese medicine, and is known to have anti-diabetic and diuretic effects.
METHODS AND RESULTS:
In this study, we evaluated the anti-inflammatory effects of Anemarsaponin B (ASB), a steroidal saponin isolated from the rhizomes of A. asphodeloides (Liliaceae), in LPS-stimulated RAW 264.7 macrophage cell line. ASB significantly and dose-dependently decreased the protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). ASB also reduced the expressions and productions of pro-inflammatory cytokines, including those of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Electrophoretic mobility shift assay (EMSA) and reporter gene assays revealed that ASB attenuated the LPS-induced DNA binding and transcriptional activity of nuclear factor-kappa B (NF-kappaB). In addition, it was found that pretreatment with ASB significantly inhibited the nuclear translocation of the p65 subunit of NF-kappaB by blocking the phosphorylation of inhibitory kappa B-alpha (IkappaB-alpha). On the other hand, ASB inhibited the phosphorylation of MAP kinase kinases 3/6 (MKK3/6) and mixed lineage kinase 3 (MLK3), which are both involved in the p38 pathway.
CONCLUSIONS:
Taken together, these results suggest that anti-inflammatory effect of ASB in LPS-treated RAW 264.7 macrophages is associated with the inhibition of NF-kappaB transcriptional activity, possibly via the p38 MAP kinase pathway.
