|Description:||1. Oridonin inhibits the growth of CEM cells in time, has no inhibitory effect on AKT kinase.|
2. Oridonin inhibits tumor growth in glioma by inducing cell cycle arrest and apoptosis, inhibits BxPC-3 cell growth through cell apoptosis.
3. Oridonin has anticancer activity, might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.
|Targets:||CDK | PARP | Caspase | mTOR | RAF | ERK | STAT | Bcl-2/Bax | JNK | p38MAPK|
|Source:||The herb of Rabdosia rubescens (Hamst.) C.Y.Wu et Hsuan|
|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.
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|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||2.744 mL||13.7201 mL||27.4401 mL||54.8802 mL||68.6003 mL|
|5 mM||0.5488 mL||2.744 mL||5.488 mL||10.976 mL||13.7201 mL|
|10 mM||0.2744 mL||1.372 mL||2.744 mL||5.488 mL||6.86 mL|
|50 mM||0.0549 mL||0.2744 mL||0.5488 mL||1.0976 mL||1.372 mL|
|100 mM||0.0274 mL||0.1372 mL||0.2744 mL||0.5488 mL||0.686 mL|
Acta Biochim Biophys Sin (Shanghai). 2015 Mar;47(3):164-73.
|Oridonin inhibits BxPC-3 cell growth through cell apoptosis.[Pubmed: 25651847]|
|The results showed that Oridonin affected cell viability in a time- and dose-dependent manner. After exposure to different Oridonin concentrations, growth rates and cell cycle arrest of BxPC-3 cells were significantly reduced compared with untreated cells, suggesting its effects on proliferation inhibition. Detailed signaling pathway analysis by western blot analysis revealed that low-dose Oridonin treatment inhibited BxPC-3 cell proliferation by up-regulating p53 and down-regulating cyclin-dependent kinase 1 (CDK1), which led to cell cycle arrest in the G2/M phase. A high-dose Oridonin not only arrested BxPC-3 cells in the G2/M phase but also induced cell accumulation in the S phase, presumably through γH2AX up-regulation and DNA damage. In addition, our results showed that a cell subpopulation was stained with propidium iodide after Oridonin treatment. Protein quantification showed that cleaved poly(ADP-ribose) polymerase (PARP) expression was increased after a high-dose Oridonin treatment, especially after long-term exposure. Accompanied by the increased level of deactivated PARP in BxPC-3 cells, the apoptosis initiators caspase-3 and caspase-7 expressions were also significantly increased, suggesting that caspase-mediated apoptosis contributed to cell death.|
Sichuan Da Xue Xue Bao Yi Xue Ban. 2014 Nov;45(6):903-7.
|Anti-leukemia effect of oridonin on T-cell acute lymphoblastic leukemia[Pubmed: 25571712]|
|Oridonin inhibited the growth of CEM cells in time- and dose dependent manner and the ICs0 of Oridonin was (7. 37± 1. 99) μmol/L after 72 h treatment. The cellular membrane of CEM cells treated with Oridonin became unsharp, some of them disintegrated. Oridonin induced apoptosis in CEM cells and the percent of apoptosis rate after 0, 5, 7.5, 10 μmol/L Oridonin treatment for 24 h were (4. 8±2. 11)%, (19.03±12.54)% ,(40.27± 3.31) / and (57. 23 ± 6. 69)% respectively. Oridonin inhibited activation of mTOR, P70S6, 4EBP1, RAF. ERK and STAT5 signaling protein, which were constitutively activated in CEM cells, however, Oridonin had no inhibitory effect on AKT kinase. Oridonin down-regulated the level of anti apoptotic protein Bcl-2 and up-regulated the expression of pro-apoptotic protein Bax.|
Zhong Yao Cai. 2014 Jul;37(7):1230-3.
|Experimental study on anti-pancreatic cancer effect of oridonin.[Pubmed: 25566662]|
|Treatment with Oridonin for 24 h resulted in a marked decrease in cell viability in a dose-dependent manner. The IC50 value was determined as 49.80 μmol/L for 24 h. After treatment with 50 micromol/L and 80 μmol/L Oridonin for 24 h, typical apoptotic nucleus alterations were observed with confocal laser scanning microscope and apoptotic rates of PANC-1 cells increased by flow cytometry analysis. Treatment with 80 μmol/L Oridonin down-regulated protein expression of JNK, p38 and increased the expression of p-JNK, p-p38. Furthermore, 80 μmol/L Oridonin treatment decreased the expression of down-stream proteins Caspase-9, Caspase-3 and PARP in the apoptotic pathway as well as activated the cleavage of Caspase-9.|
Cell Mol Biol (Noisy-le-grand). 2014 Dec 30;60(6):29-36.
|Oridonin inhibits tumor growth in glioma by inducing cell cycle arrest and apoptosis.[Pubmed: 25553351]|
|We systemically investigated the role of Oridonin in tumor growth and the underlying mechanisms in human glioma. We found that Oridonin inhibited cell proliferations in a dose- and time-dependent manner in both glioma U87 and U251 cells. Moreover, these anti-cancer effects were also confirmed in a mouse model bearing glioma. Furthermore, cell cycle arrest in S phase was observed in Oridonin-mediated growth inhibition by flow cytometry. Cell cycle arrest in S phase led to eventual cell apoptosis, as revealed by Hoechst 33342 staining and annexin V/PI double-staining. The cell apoptosis might be accomplished through a mitochondrial manner. In all, we were the first to our knowledge to report that Oridonin could exert anti-cancer effects on tumor growth in human glioma by inducing cell cycle arrest and eventual cell apoptosis. The identification of Oridonin as a critical mediator of glioma growth may potentiate Oridonin as a novel therapeutic strategies in glioma treatments.|