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].
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.
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.
*请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。
可选溶剂
浓度溶剂体积质量
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
Help & FAQs
Do most proteins show cross-species activity?
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.
Powered by Bioz
