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Beta-Sitosterol (purity>98%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc.
For research use only. We do not sell to patients.
Mice were administered β-sitosterol (75 mg/kg) each day via oral gavage. Nude mice were subcutaneously injected with MDA-MB-231 cells. Representative images showed the dissected tumors in distinct treatment groups as specified at the endpoint.
Mice were administered β-sitosterol (75 mg/kg) each day via oral gavage. Tumor lysates were collected, and the protein profile was established by immunoblotting analysis.
Beta-Sitosterol (purity>98%) is orally active. Beta-Sitosterol exhibits multiple activities, including anti-inflammatory, anticancer, antioxidant, antimicrobial, antidiabetic, antioxidant enzyme, and analgesic. Beta-Sitosterol inhibits inflammation and impaired adipogenesis in bovine mammary epithelial cells by reducing levels of ROS, TNF-α, IL-1β, and NF-κB p65 and restoring the activity of the HIF-1α/mTOR signaling pathway. Beta-Sitosterol induces apoptosis in cancer cells through ROS-mediated mitochondrial dysregulation and p53 activation. Beta-Sitosterol exerts its anticancer effects in cancer cells by activating caspase-3, caspase-8, and caspase-9, mediating PARP inactivation, MMP loss, altered Bcl-2-Bax ratio, and cytochrome c release. Beta-Sitosterol modulates macrophage polarization and reduces rheumatoid inflammation in mice. Beta-Sitosterol inhibits tumor growth in multiple mouse cancer models. Beta-Sitosterol can be used in the research of arthritis, lung cancer, breast cancer and other cancers, diabetes, etc[1][2][3][4][5][6][7][8][9][10].
Beta-Sitosterol (0-40 µM, 24 h) decreases cell viability with concentrations exceeding 5 µM in MAC-T cells
[1].
Beta-Sitosterol (1 µM, 24 h) increases the levels of CAT, GSH, T-AOC, T-SOD and decreases the level of ROS, TNF-α, IL-1β, NF-κB p65 in LPS (HY-D1056)-induced MAC‐T cells[1].
Beta-Sitosterol (1 µM, 24 h) inhibits apoptosis, attenuates the expression levels of caspase-3 and Bax, increases the levels of Bcl-2 and Bcl-2/Bax radio in LPS-induced MAC‐T cells[1].
Beta-Sitosterol (1 µM, 24 h) restores HIF-1α/mTOR signaling pathway viability and the expression of fat synthesis-related Genes (SCD, PSMA5, FASN, SREBP1) in LPS-induced MAC-T cells[1].
Beta-Sitosterol (25-200 µM, 24-72 h) affectes the growth of A549 cells, with an IC50 of 24.7 μM at 72 h, increases the release of LDH in A549 cells, affects the viability of NCI-H460 cells, but does not affect the growth and viability of normal human lung, PBMC cells and NCI-H23 cells[2].
Beta-Sitosterol (25-200 µM, 24-72 h) induces cell cycle arrest at Sub-G1 phase, reduces the expression of Cyclin D1 and CDK2 in A549 cells[2].
Beta-Sitosterol (25-200 µM, 0-72 h) induces apoptosis occurred via mitochondrial dysfunction and ROS mediated DNA damage in A549 cells[2].
Beta-Sitosterol (25-200 µM, 0-72 h) elevates the expression levels of caspase-3, caspase-9, cleavage PARP, Bax, p53 and pSer15-p53, suppresses the expression levels of Bcl-2 in A549 cells[2].
Beta-Sitosterol (25-200 µM, 72 h) induces apoptosis occurred via the activation of p53 in NCI-H460 cells[2].
Beta-Sitosterol decreases the expression of both TrxR1 and Trx1 in A549 and NCI-H460 cells[2].
Beta-Sitosterol (5-50 µM, 24 h) blocks M1 but promotes M2 macrophage polarization in IFN-γ/IL-4-stimulated BMBMs[3].
Beta-Sitosterol (1-150 μM/L, 5 days) increases MCF-7 cells proliferation[5].
Beta-Sitosterol (8-16 μM, 5 days) causes a significant reduction in cell growth, alters composition of cell membranes in MCF-7 and MDA-MB-231 cells[6].
Beta-Sitosterol (16 μM, 1-3 days) increases caspase-8 activity and Fas protein levels in MCF-7 and MDA-MB-231 cells[6].
Beta-Sitosterol (0.1-100 μM, 18 h) reduces VCAM-1 and ICAM-1 expression, attenuates phosphorylation of NFkB p65 in TNF-α- stimulated HAEC, inhibits binding of U937 cells to TNF-α-stimulated HAEC[7].
Beta-Sitosterol (50 μM, 1-6 h) reverts the enhancement of GSSG levels and the impairment of GSH levels or the GSH/total glutathione ratio induced by PMA (HY-18739) in RAW 264.7 cells[8].
Beta-Sitosterol (50 μM, 1-6 h) increases GPx and Mn SOD activities, and decreases catalase activity in RAW 264.7 cells[8].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Slowed the mRNA expression levels of pro-inflammatory factors TNF-α and IL-1β down.
Upregulated the mRNA levels of HIF-1α and mTOR.
Restored the mRNA expression of fatty acid synthase (FASN) and sterol regulatory element-binding protein 1 (SREBP1) to the controls.
Attenuated NF-κB p65 production by LPS-induced and restored it to the same level as the control group.
Upregulated the protein expression of HIF-1α and the ratio of p-mTOR/mTOR.
Restored the protein expression of stearoyl coenzyme A dehydrogenase (SCD), proteasome 20 s subunit α5 (PSMA5) to the controls.
Inhibited the apoptosis caused by LPS, attenuated the expression levels of mRNA and protein of caspase-3 and pro-apoptotic protein B-cell lymphoma-2-associated X protein (Bax), increased the protein levels of Bcl-2 and Bcl-2/Bax radio.
Increased early apoptotic cells and few late apoptotic cells upon 25μM exposure, elevated the protein expression levels of caspase-3, caspase-9, cleavage PARP.
Induced a concentration dependent disruption of ΔΨm afer 72h treatment, induced the release of cytochrome c into the cell cytoplasm in a dose dependent manner, suppressed the Bcl-2 and strongly increased the expression of Bax in a dose dependent manner.
Induced generation of DCF fuorescence at 6h of BS treatment and peaked at 12-48h time point, decreased at 72 h, caused severe DSBs and elevation of tail and olive movement, caused chromatin condensation and morphological alteration.
Up-regulated the protein expression of p53 and pSer15-p53.
Induced cell shrinkage, elongation and reduced cell populations, elevated the protein expression levels of caspase-3, caspase-9, cleavage PARP.
Reduced the expression of Bcl-2 protein and signifcant elevated Bax and cytochrome c, up-regulated p53, pSer15-p53 and p21 expression.
Decreased NOS and IL-1β to 50.2% and 47.1% at 25 μM in the presence of IFN-γ, and increased the expression of arginase-1 by approximately 0.5-fold and IL-10 by approximately 1-fold in the presence of IL-4, compared with vehicle-treated BMDMs.
Significantly dose-dependent reduced VCAM-1 and ICAM-1 expression.
In Vivo
Beta-Sitosterol (20-50 mg/kg, i.p., every 2 days, 31 days; 2 × 106 BMDMs treating with 25 μM BS, i.v., once) inhibits pathological changes by suppressing humoral and cellular immune responsesin, in part, through IL-10 transfer in Collagen (HY-NP003)-induced arthritis (CIA) mice model[3].
Beta-Sitosterol (2-5 mg/20 g mouse, i.p., once) plays an analgesic role in Acetic acid (HY-Y0319)-induced Swiss Webster albino mice model[4].
Beta-Sitosterol (2 mg/20 g mouse, i.p., once) plays an anti-inflammatory role in Carrageenan (HY-125474)-induced mouse paw oedema model[4].
Beta-Sitosterol (9.8 g/kg diet, o.p., 18 weeks) inhibits the growth of estrogen-responsive breast cancer cells of MCF-7 tumors implanted in ovariectomized athymic mice[5].
Beta-Sitosterol (10-20 mg/kg, o.p., once a day, 21 days) has antidiabetic as well as antioxidant effects in Streptozotocin (HY-13753)-induced diabetes Wistar rats model[9].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Suppressed hind paw swelling and the production of collagen-specific IgG and IgG1, but not IgG2c.
Decreased IL-1β, IL-6, and IL-12 levels and increased IL-10 levels.
2 × 106 BMDMs treating with 25 μM BS + 30 μg LPS, i.p., on day 3
Administration:
i.v., once
Result:
Reduced ankle swelling and synovial inflammation, reduced serum collagen-specific IgG, IgG1, and IgG2a antibodies, as well as IL-1β and IL-6, and increased serum IL-10 levels.
Did not affect tumor growth, regressed tumors after removal of the E2 pellet at wk 7, reduced 1:47 E2-induced tumor growth by 38.9%.
Downregulated Bcl-2 expression in the 1:47 E2 group by 38%, lowered the serum E2 level in the 1:47 E2 group by 35.1%.
Reduced blood glucose (37.5%, 45.2%, and 50.4% in diabetic rats) and NO (16.4%, 28.4%, and 47.1% in diabetic rats).
Prevented the induction of diabetes by 77.8% and 100% at 10, 15 mg/kg, increased insulin levels and lowered HbA1c levels, dose-dependent increased pancreatic protein content.
Improved antioxidant activity and significantly reduced LPO levels, caused the pancreatic cells to rejuvenate.
Ethanol : 5 mg/mL (12.06 mM; ultrasonic and warming and heat to 60°C)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
2.4113 mL
12.0566 mL
24.1132 mL
5 mM
0.4823 mL
2.4113 mL
4.8226 mL
10 mM
0.2411 mL
1.2057 mL
2.4113 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Protocol 1
Add each solvent one by one: 10% EtOH 40% PEG300 5% Tween-80 45% Saline
This protocol yields a suspended solution of ≥ 1 mg/mL (saturation unknown). Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL EtOH stock solution (10.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% EtOH 90% (20% SBE-β-CD in Saline)
Solubility: 1 mg/mL (2.41 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 1 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL EtOH stock solution (10.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
Protocol 3
Add each solvent one by one: 10% EtOH 90% Corn Oil
Solubility: ≥ 1 mg/mL (2.41 mM); Clear solution
This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μL EtOH stock solution (10.0 mg/mL) to 900 μLCorn oil, and mix evenly.
For the following dissolution methods, please prepare the working solution directly.
It is recommended to prepare fresh solutions and use them promptly within a short period of time. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution.
If precipitation or phase separation occurs during preparation,
heat and/or sonication can be used to aid dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Optional Solvent
ConcentrationSolventMass
1 mg
5 mg
10 mg
25 mg
Ethanol
1 mM
2.4113 mL
12.0566 mL
24.1132 mL
60.2831 mL
5 mM
0.4823 mL
2.4113 mL
4.8226 mL
12.0566 mL
10 mM
0.2411 mL
1.2057 mL
2.4113 mL
6.0283 mL
Beta-Sitosterol (purity>98%) Related Classifications
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
Customer Validation
Mice were administered β-sitosterol (75 mg/kg) each day via oral gavage. Nude mice were subcutaneously injected with MDA-MB-231 cells. Representative images showed the dissected tumors in distinct treatment groups as specified at the endpoint.
Customer Validation
Mice were administered β-sitosterol (75 mg/kg) each day via oral gavage. Tumor lysates were collected, and the protein profile was established by immunoblotting analysis.
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