|Source:||The seeds of Schisandra chinensis (Turcz.) Baill.|
|Biological Activity or Inhibitors:||1. Schizandrin B can enhance cell survival via reducing apoptosis rate on HK-2 cells along four processes that could help alleviate CisPt toxicity, thus, it presents promising activities for future development of protective agents against CisPt nephrotoxicity.
2. Schizandrin B possesses antioxidant activity, it can decrease the production of MDA and the release of GPT and LDH, and to increase hepatocyte viability as well as maintaining the integrity of the hepatocyte membrane surface.
3. Schizandrin B attenuates the UVB-induced toxicity of HaCaT by inhibiting apoptotic gene expression,it plays a role in anti-photoaging.
4. Schisandrin B can partially inhibit H2O2-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.
5. Combination of schizandrin B and paclitaxel(PTX) can enhance anti-tumor effects and relieve side effects of PTX on rats with mammary carcinoma.
|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: 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||2.4971 mL||12.4853 mL||24.9707 mL||49.9413 mL||62.4266 mL|
|5 mM||0.4994 mL||2.4971 mL||4.9941 mL||9.9883 mL||12.4853 mL|
|10 mM||0.2497 mL||1.2485 mL||2.4971 mL||4.9941 mL||6.2427 mL|
|50 mM||0.0499 mL||0.2497 mL||0.4994 mL||0.9988 mL||1.2485 mL|
|100 mM||0.025 mL||0.1249 mL||0.2497 mL||0.4994 mL||0.6243 mL|
J Appl Toxicol. 2014 Dec;34(12):1311-9.
|Protective effects of schizandrin and schizandrin B towards cisplatin nephrotoxicity in vitro.[Pubmed: 24155209]|
|Renal proximal tubular epithelial cells are the main targets of toxic drugs such as cisplatin (CisPt), an alkylating agent indicated for the treatment of solid organ tumors. Current techniques aiming at reducing nephrotoxicity in patients receiving CisPt are still not satisfactory as they can only partially prevent acute kidney injury. New nephroprotective strategies remain to be developed. In the present in vitro study, schizandrin (Schi) and Schizandrin B (Schi B), major phytochemicals from Schisandra chinensis (Turcz.) Baill. fruits, were tested on HK-2 cells along four processes that could help alleviate CisPt toxicity. Results indicated that: (i) both Schi and Schizandrin B enhanced cell survival via reducing apoptosis rate; (ii) only Schi showed moderate effects towards modulation of regeneration capacities of healthy cells; (iii) both Schi and Schizandrin B limited extracellular matrix deposition; and (iv) both compounds could help preventing dedifferentiation processes via the β-catenin pathway. Schi and Schi B present promising activities for future development of protective agents against CisPt nephrotoxicity.|
Nan Fang Yi Ke Da Xue Xue Bao. 2012 Apr;32(4):583-5, 592.
|[Effect of schizandrin B on H(2)O(2)-induced apoptosis of human hepatocytes in vitro: role of Fas pathway].[Pubmed: 22543149]|
|OBJECTIVE: To investigate the role of Fas pathway in H(2)O(2)-induced apoptosis of L02 human hepatocytes and the effect of Schizandrin B on Fas pathway. METHODS: Real-time quantitative PCR was used to detect the expressions of FAS, fas associated death domain protein (FADD) and caspase-8 mRNA in L02 cells exposed to H(2)O(2). Flow cytometry was employed to assess the cell apoptosis. ELISA, Western blotting and spectrophotometric assay were performed to determine the expressions of FAS protein, FADD protein and caspase-8 activity. RESULTS: Within the dose range of 5-15 mol/L, Schizandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation. CONCLUSION: Schizandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.|
Chinese Pharmacological Bulletin, 2014, 30(4):523-7.
|Protective effect of schizandrin B against oxidative damage of UVB irradiated HaCaT cells and its molecular mechanism.[Reference: WebLink]|
|To investigate the inhibitory effect of Schizandrin B( SchB) on ultraviolet radiation b( UVB)radiation-induced apoptosis of HaCaT cells. Methods Methyl thiazolyl tetrazolium( MTT) assay was used to examine the effect of SchB on cell viability recovery.Cell apoptosis and necrosis were measured by Hochest33342 staining. The p53, p21 and Caspase-3mRNA expressions were examined by RT-PCR. Results In this study,we found that Sch B attenuated UVB-induced toxicity in HaCaT cells. Through Hoechst 33342stain,we visualized that SchB could inhibit UVB-induced HaCaT cell death. The result demonstrated that p53,p21 and Caspase-3 mRNA levels decreased compared with the control group. Conclusions Sch B at-tenuates the UVB-induced toxicity of HaCaT by inhibiting apoptotic gene expression. It plays a role in antiphotoaging.|
J. Pract. Med., 2012, 28(15):2506-9.
|Experimental research on Schizandrin B enhancing sensitivity to paclitaxel on rats with mammary carcinoma.[Reference: WebLink]|
|To investigate the effects of Schizandrin B (Sch B) on enhancing sensitivity to paclitaxel (PTX) on rats with mammary carcinoma. Methods Fifty BALB/c rats were randomly divided into five groups, 10 animals of each group: a normal control (NC) group, model control (MC) group, PTX group, Sch B group and PTX + Sch B group. Sch B was administered to the rats by intraperitoneal injection at a dose of 10mg/kg once per day for 22 days. while PTX was every 2 days. The body weight, gross tumor volume, inhibition rate of tumor growth and organ index were observed. Results Compared with the MC group, the body weight in both the PTX group and Sch B + PTX group began to decrease since the 7th day of administration, the difference in weight was significant by statistics. Compared with the PTX group, the body weight in the Sch B + PTX group was elevated, but the difference was not significant. The inhibition rate in the PTX group was 15.7% and that in the Sch B + PTX group 25.9%. Compared with the MC group, the spleen index in PTX group and the Sch B + PTX group was significantly lower (P = 0.008 and 0.000, respectively). Compared with the PTX group, the spleen index in the Sch B + PTX group was lower, but the difference was not significant. Compared with the PTX group, the thyroid and adrenal gland index in the Sch B + PTX group was significantly elevated (P = 0.000 and 0.011, respectively). Conclusions Combination of Sch B and PTX can enhance anti-tumor effects and relieve side effects of PTX on rats with mammary carcinoma.|
Zhongguo Yao Li Xue Bao. 1989 Jul;10(4):353-6.
|Action of schizandrin B, an antioxidant, on lipid peroxidation in primary cultured hepatocytes.[Pubmed: 2624122]|
|The action of Schizandrin B (Sin B) was observed in freshly isolated hepatocytes damaged by FeSO4/cysteine and CCl4. Two types of free radicals, .OH and .CCl3, generated from FeSO4/cysteine and CCl4, respectively, induced lipid peroxidation in hepatocytes. It was found that the speed of lipid peroxidation (MDA production) and the degree of alteration in hepatocyte morphology were closely related to the type of free radicals. MDA production and membrane protrusion of hepatocytes injuries by FeSO4/cysteine were faster and more severe than those observed with CCl4. Sin B was shown to decrease the production of MDA and the release of GPT and LDH, and to increase hepatocyte viability as well as maintaining the integrity of the hepatocyte membrane surface. These actions of Sin B were stronger than vitamin E at the same concentration. It was observed that no inhibitory effect of phenobarbital, a typical inducer of cytochrome P-450, as Sin B induced liver cytochrome P-450, on MDA production in hepatocytes damaged by FeSO4/cysteine. The results suggest that Sin B possesses antioxidant activity.|