|Description:||1. Glaucocalyxin B alleviates lipopolysaccharide-induced Parkinson's disease by inhibiting TLR/NF-κB and activating Nrf2/HO-1 Pathway. |
2. Glaucocalyxin B is a potent NF-κB inhibitor for Alzheimer's disease treatment.
3. Glaucocalyxin B shows sensitization of gastric cancer cells to alkylating agents via cell cycle arrest and enhances cell death.
4. Glaucocalyxin B induces apoptosis and autophagy in human cervical cancer cells.
5. Glaucocalyxin B has anti-inflammatory effects, it exhibits neuroprotective effect by preventing over-activated microglia induced neurotoxicity in a microglia/neuron co-culture model.
|Targets:||TLR | NF-kB | HO-1 | Nrf2 | IkB | PARP | Akt | Autophagy | COX | NO | TNF-α | IL Receptor | NOS | ROS | p38MAPK | IKK|
|Source:||The herbs of Rabdosia rubescens.|
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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: firstname.lastname@example.org
|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||2.6704 mL||13.3522 mL||26.7044 mL||53.4088 mL||66.761 mL|
|5 mM||0.5341 mL||2.6704 mL||5.3409 mL||10.6818 mL||13.3522 mL|
|10 mM||0.267 mL||1.3352 mL||2.6704 mL||5.3409 mL||6.6761 mL|
|50 mM||0.0534 mL||0.267 mL||0.5341 mL||1.0682 mL||1.3352 mL|
|100 mM||0.0267 mL||0.1335 mL||0.267 mL||0.5341 mL||0.6676 mL|
Cell Physiol Biochem. 2017;44(6):2091-2104.
|Glaucocalyxin B Alleviates Lipopolysaccharide-Induced Parkinson's Disease by Inhibiting TLR/NF-κB and Activating Nrf2/HO-1 Pathway.[Pubmed: 29241205]|
|Parkinson's disease (PD) is a common neurodegenerative disease in the old population, characterized by dopaminergic neuron loss, inflammation and oxidative stress injury in the substantia nigra. Glaucocalyxin B (GLB), an ent-kauranoid diterpenoid isolated from Rabdosia japonica, has anti-inflammation and anti-tumor effects. However, its effects on PD remain unclear. METHODS: PD was introduced in rats via injection of lipopolysaccharide (LPS) into cerebral corpus striatum, and GLB was given intracerebroventricularly to these rats. Their walking, climbing and sensory states were detected by Stepping, Whisker and Cylinder Tests. The expression of tyrosine hydroxylase (TH), glial fibrillary acidic protein (GFAP), CD11b and ionized calcium binding adaptor molecule (IBA)-1 were detected by immunohischemical staining. The levels of a series of inflammatory factors, oxidative stress-related factors and apoptosis-related factors were measured by real-time PCR, immunoblotting and ELISA. In addition, Toll-like receptor (TLR)/nuclear factor kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 pathways were investigated to illustrate the underlying mechanism. In vitro, microglial cells exposed to LPS were treated with GLB. RESULTS: The injection of LPS caused walking, climbing and sensory disturbances in rats, induced inflammation, oxidative stress response and apoptosis, and activated TLR/NF-κB and Nrf2/ HO-1 pathways in the cerebral tissue. GLB administration attenuated LPS-induced alterations. The TLR/NF-κB pathway was deactivated and Nrf2/HO-1 was activated after application of GLB. In vitro, cytotoxic effects induced by the conditioned medium derived from microglial cells exposed to LPS in PC12 cells were attenuated by GLB. CONCLUSION: GLB suppresses LPS-induced PD symptoms by modification of TLR/NF-κB and Nrf2/HO-1 pathways in vivo and in vitro.|
Pharmacol Res. 2018 Mar;129:262-273.
|Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer's disease.[Pubmed: 29179999 ]|
|Alzheimer's disease (AD) is the most prevalent form of dementia. The exact pathophysiology of this disease remains incompletely understood and safe and effective therapies are required. AD is highly correlated with neuroinflammation and oxidative stress in brain causing neuronal loss. Nuclear factor of activated B-cells (NF-κB) is involved in physiological inflammatory processes and thus representing a promising target for inflammation-based AD therapy. Phytochemicals are able to interfere with the NF-κB pathway. They inhibit the phosphorylation or the ubiquitination of signaling molecules, and thus, inhibit the degradation of IκB. The translocation of NF-κB to the nucleus and subsequent transcription of pro-inflammatory cytokines are inhibited by the actions of phytochemicals. Additionally, natural compounds preventing the interaction of NF-κB can block NF-κB's transcriptional activity by inhibiting its binding to target DNA. Many polyphenols including curcumin, resveratrol, pterostilbene, punicalagin, macranthoin G, salidroside, 4-O-methylhonokiol, lycopene, genistein, obovatol and gallic acid were reported as potent NF-κB inhibitors for AD treatment. Several alkaloids such as galantamine, Glaucocalyxin B, tetrandrine, berberine, oridonin, anatabine have been shown anti-inflammatory effects in AD models in vitro as well as in vivo. Besides, vitamins, tanshinone IIA, artemisinin, dihydroasparagusic acid, geniposide, xanthoceraside, l-theranine, 1,8-cineole and paeoniflorin were described as promising NF-κB inhibitors. In conclusion, natural products from plants represent interesting candidates for AD treatment. They may qualify as promising compounds for the development of derivatives providing enhanced pharmacological features.|
Drug Des Devel Ther. 2017 Aug 22;11:2431-2441.
|Sensitization of gastric cancer cells to alkylating agents by glaucocalyxin B via cell cycle arrest and enhanced cell death.[Pubmed: 28860714]|
|Severe side effects are major problems with chemotherapy of gastric cancer (GC). These side effects can be reduced by using sensitizing agents in combination with therapeutic drugs. In this study, the low/nontoxic dosage of Glaucocalyxin B (GLB) was used with other DNA linker agents mitomycin C (MMC), cisplatin (DDP), or cyclophosphamide (CTX) to treat GC cells. Combined effectiveness of GLB with drugs was determined by proliferation assay. The molecular mechanisms associated with cell proliferation, migration, invasion, cell cycle, DNA repair/replication, apoptosis, and autophagy were investigated by immunoblotting for key proteins involved. Cell cycle and apoptosis analysis were performed by flow cytometry. Reactive oxygen species level was also examined for identification of its role in apoptosis. Proliferation assay revealed that the addition of 5 μM GLB significantly sensitizes gastric cancer SGC-7901 cells to MMC, DDP, and CTX by decreasing half-maximal inhibitory concentration (IC50) by up to 75.40%±5%, 45.10%±5%, and 52.10%±5%, respectively. GLB + drugs decreased the expression level of proteins involved in proliferation and migration, suggesting the anticancer potential of GLB + drugs. GLB + MMC, GLB + CTX, and GLB + DDP arrest the cells in G0/G1 and G1/S phase, respectively, which may be the consequence of significant decrease in the level of enzymes responsible for DNA replication and telomerase shortening. Combined use of GLB with these drugs also induces DNA damage and apoptosis by activating caspase/PARP pathways and increased production of reactive oxygen species and increased autophagy in GC cells. GLB dosage sensitizes GC cells to the alkylating agents via arresting the cell cycle and enhancing cell death. This is of significant therapeutic importance in the reduction of side effects associated with these drugs.|
Mol Med Rep. 2016 Aug;14(2):1751-5.
|Glaucocalyxin B induces apoptosis and autophagy in human cervical cancer cells.[Pubmed: 27356884]|
|Glaucocalyxin (Gln), an ent‑kaurane diterpenoid isolated from the Chinese traditional medicine, Rabdosia japonica, represents a novel class of anticancer drugs. Glaucocalyxin A(GlnA) is one of the three major forms of Gln and has demonstrated potent anticancer effects in a variety of cancer types. Glaucocalyxin B(GlnB) has only one structural difference from GlnA, an acetylated hydroxyl group at C14. This acetyl group results in high liposolubility and may enhance the antitumor activity of ent‑kaurane diterpenoid GlnB. However, few studies have reported the role of GlnB in cancer. The present study investigated the effect of GlnB in cervical cancer proliferation and cell death. Treatment with GlnB inhibits the proliferation of HeLa and SiHa cervical cancer cell lines in a dose‑dependent manner, as assessed by 3‑(4,5‑dimethylthiazol-2‑yl)-2,5 diphenyl tetrazolium bromide assays. In addition, GlnB increases the apoptotic cell population of HeLa and SiHa cells, as determined by fluorescence‑activated cell sorting analysis and enhanced poly (ADP‑ribose) polymerase 1 cleavage by western blotting. GlnB also induces increased light chain 3 II/I protein cleavage in both cells, indicating the induction of autophagy. Furthermore, GlnB treatment increased the expression of phosphatase and tensin homolog and decreased the expression of phosphorylated‑protein kinase B (Akt) in HeLa and SiHa cells, as assessed by western blotting. Taken together, the present results demonstrated that GlnB inhibited the proliferation of human cervical cancer cells in vitro through the induction of apoptosis and autophagy, which may be mediated by the phosphatidylinositol‑4,5‑bisphosphate 3‑kinase/Akt signaling pathway.|
J Pharmacol Sci. 2015 May;128(1):35-46.
|Anti-inflammatory effects of glaucocalyxin B in microglia cells.[Pubmed: 26003084]|
|Over-activated microglia is involved in various kinds of neurodegenerative process including Parkinson, Alzheimer and HIV dementia. Suppression of microglial over activation has emerged as a novel strategy for treatment of neuroinflammation-based neurodegeneration. In the current study, anti-inflammatory and neuroprotective effects of the ent-kauranoid diterpenoids, which were isolated from the aerial parts of Rabdosia japonica (Burm. f.) var. glaucocalyx (Maxim.) Hara, were investigated in cultured microglia cells. 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. In addition, GLB inhibited activation of nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (MAPK) and generation of reactive oxygen species (ROS) in LPS-activated microglia cells. Furthermore, GLB strongly induced the expression of heme oxygenase (HO)-1 in BV-2 microglia cells. Finally, GLB exhibited neuroprotective effect by preventing over-activated microglia induced neurotoxicity in a microglia/neuron co-culture model. Taken together, the present study demonstrated that the GLB possesses anti-nueroinflammatory activity, and might serve as a potential therapeutic agent for treating neuroinflammatory diseases.|