|Description:||1. Saikosaponin D shows potent anti-inflammatory activity through inhibitory effects on NF-κB activation and thereby on iNOS, COX-2 and pro-inflammatory cytokines.|
2. Saikosaponin D protects against acetaminophen-induced hepatotoxicity by inhibiting NF-κB and STAT3 signaling.
3. Saikosaponin D, a novel SERCA inhibitor, induces autophagic cell death in apoptosis-defective cells.
4. Saikosaponin D ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK1 cells.
5. Saikosaponin D inhibits proliferation of human undifferentiated thyroid carcinoma cells through induction of apoptosis and cell cycle arrest.
6. Saikosaponin D is an agonist of the glucocorticoid receptor (GR), and it possesses neuroprotective effects in corticosterone-treated PC12 cells.
|Targets:||p53 | Bcl-2/Bax | p21 | CDK | NF-kB | STAT | SOD | HSP (e.g. HSP90) | Glucocorticoid Receptor | Calcium Channel | ATPase | AMPK | NOS | COX | NO | PGE | TNF-α | IL Receptor|
|Source:||The herb of Bupleurum chinense DC.|
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.2804 mL||6.4021 mL||12.8043 mL||25.6085 mL||32.0107 mL|
|5 mM||0.2561 mL||1.2804 mL||2.5609 mL||5.1217 mL||6.4021 mL|
|10 mM||0.128 mL||0.6402 mL||1.2804 mL||2.5609 mL||3.2011 mL|
|50 mM||0.0256 mL||0.128 mL||0.2561 mL||0.5122 mL||0.6402 mL|
|100 mM||0.0128 mL||0.064 mL||0.128 mL||0.2561 mL||0.3201 mL|
Eur Rev Med Pharmacol Sci. 2014;18(17):2435-43.
|Saikosaponin-d inhibits proliferation of human undifferentiated thyroid carcinoma cells through induction of apoptosis and cell cycle arrest.[Pubmed: 25268087]|
|In vitro, MTT assay showed that Saikosaponin D treatment inhibited cell proliferation in three human anaplastic thyroid cancers cell lines ARO, 8305C and SW1736. In addition, Saikosaponin D promoted cell apoptosis and induced G1-phase cell cycle arrest as shown by flow cytometric analysis. On the molecular level, our results showed that Saikosaponin D treatment increased the expression of p53 and bax, and decreased the expression of Bcl-2. In addition, Saikosaponin D administration led to a significant up-regulation of p21 and down-regulation of CDK2 and cyclin D1. Xenografts tumorigenesis model demonstrated that Saikosaponin D markedly reduced the weight and volume of thyroid tumors in vivo|
Chem Biol Interact. 2014 Sep 27;223C:80-86.
|Saikosaponin d protects against acetaminophen-induced hepatotoxicity by inhibiting NF-κB and STAT3 signaling.[Pubmed: 25265579]|
|Biochemical and pathological analysis revealed that mice treated with Saikosaponin D were protected against APAP-induced hepatotoxicity. Saikosaponin D markedly suppressed phosphorylation of nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) and reversed the APAP-induced increases in the target genes of NF-κB, such as pro-inflammatory cytokine Il6 and Ccl2, and those of STAT3, such as Socs3, Fga, Fgb and Fgg. SSd also enhanced the expression of the anti-inflammatory cytokine Il10 mRNA. Collectively, these results demonstrate that Saikosaponin D protects mice from APAP-induced hepatotoxicity mainly through down-regulating NF-κB- and STAT3-mediated inflammatory signaling. This study unveils one of the possible mechanisms of hepatoprotection caused by Bupleurum falcatum and/or Saikosaponin D.|
Am J Chin Med. 2014;42(5):1261-77.
|Saikosaponin-D attenuates heat stress-induced oxidative damage in LLC-PK1 cells by increasing the expression of anti-oxidant enzymes and HSP72.[Pubmed: 25169909]|
|DNA ladder and MTT assays demonstrated that SSd helped to prevent heat stress-induced cellular damage when compared to untreated cells. Additionally, pretreatment with SSd increased the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) but decreased the concentration of malondialdehyde (MDA) in a dose-dependent manner when compared to controls. Furthermore, real-time PCR and Western blot analysis demonstrated that Saikosaponin D significantly increased the expression of copper and zinc superoxide dismutase (SOD-1), CAT, GPx-1 and heat shock protein 72 (HSP72) at both the mRNA and protein levels. In conclusion, these results are the first to demonstrate that Saikosaponin D ameliorates heat stress-induced oxidative damage by modulating the activity of anti-oxidant enzymes and HSP72 in LLC-PK1 cells.|
Prog Neuropsychopharmacol Biol Psychiatry. 2014 Aug 4;53:80-9.
|Saikosaponin D acts against corticosterone-induced apoptosis via regulation of mitochondrial GR translocation and a GR-dependent pathway.[Pubmed: 24636912]|
|Saikosaponin D is an agonist of the glucocorticoid receptor (GR), and our preliminary study showed that it possesses neuroprotective effects in corticosterone-treated PC12 cells.
These additional data suggested that Saikosaponin D partially reversed the physiological changes induced by corticosterone by inhibiting the translocation of the GR to the mitochondria, restoring mitochondrial function, down-regulating the expression of pro-apoptotic-related signalling events and up-regulating anti-apoptotic-related signalling events. These findings suggest that Saikosaponin D exhibited its anti-apoptotic effects via differential regulation of mitochondrial and nuclear GR translocation, partial reversal of mitochondrial dysfunction, inhibition of the mitochondrial apoptotic pathway, and selective activation of the GR-dependent survival pathway.
Cell Death Dis. 2013 Jul 11;4:e720.
|Saikosaponin-d, a novel SERCA inhibitor, induces autophagic cell death in apoptosis-defective cells.[Pubmed: 23846222 ]|
|Autophagy is an important cellular process that controls cells in a normal homeostatic state by recycling nutrients to maintain cellular energy levels for cell survival via the turnover of proteins and damaged organelles. However, persistent activation of autophagy can lead to excessive depletion of cellular organelles and essential proteins, leading to caspase-independent autophagic cell death. As such, inducing cell death through this autophagic mechanism could be an alternative approach to the treatment of cancers. Recently, we have identified a novel autophagic inducer, Saikosaponin D (Ssd), from a medicinal plant that induces autophagy in various types of cancer cells through the formation of autophagosomes as measured by GFP-LC3 puncta formation. By computational virtual docking analysis, biochemical assays and advanced live-cell imaging techniques, Ssd was shown to increase cytosolic calcium level via direct inhibition of sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, leading to autophagy induction through the activation of the Ca(2+)/calmodulin-dependent kinase kinase-AMP-activated protein kinase-mammalian target of rapamycin pathway. In addition, Ssd treatment causes the disruption of calcium homeostasis, which induces endoplasmic reticulum stress as well as the unfolded protein responses pathway. Ssd also proved to be a potent cytotoxic agent in apoptosis-defective or apoptosis-resistant mouse embryonic fibroblast cells, which either lack caspases 3, 7 or 8 or had the Bax-Bak double knockout. These results provide a detailed understanding of the mechanism of action of Ssd, as a novel autophagic inducer, which has the potential of being developed into an anti-cancer agent for targeting apoptosis-resistant cancer cells.|
Int Immunopharmacol. 2012 Sep;14(1):121-6.
|Saikosaponin a and its epimer saikosaponin d exhibit anti-inflammatory activity by suppressing activation of NF-κB signaling pathway.[Pubmed: 22728095 ]|
|Saikosaponin a (SSa) and its epimer Saikosaponin D (SSd) are major triterpenoid saponin derivatives from Radix bupleuri (RB), which has been long used in Chinese traditional medicine for treatment of various inflammation-related diseases. In the present study, the anti-inflammatory activity, as well as the underlying mechanism, of SSa and SSd was investigated in lipopolysaccharide (LPS)-induced RAW264.7 cells. Our results demonstrated that both SSa and SSd significantly inhibited the expression of inducible nitric-oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-induced RAW264.7 cells, and finally resulted in the reduction of nitric oxide (NO) and prostaglandin E(2) (PGE(2)). In addition, LPS-induced production of major pro-inflammatory cytokines: the tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), was suppressed in a dose-dependent manner by the treatment of SSa or SSd in RAW264.7 cells. Further analysis revealed that both SSa and SSd could inhibit translocation of nuclear factor-κB (NF-κB) from the cytoplasm to the nucleus in the LPS-induced RAW264.7 cells. Furthermore, SSa and SSd exhibited significant anti-inflammatory activity in two different murine models of acute inflammation, carrageenan-induced paw edema in rats and acetic acid-induced vascular permeability in mice. In conclusion, SSa and SSd showed potent anti-inflammatory activity through inhibitory effects on NF-κB activation and thereby on iNOS, COX-2 and pro-inflammatory cytokines.|