Product name: Schizandrol B
Synonym name: schisandrol B; Wuweizi alcohol B; Besigomsin; Wuweizi alcohol B; Gomisin A
Catalogue No.: BP1266
Cas No.: 58546-54-6
Formula: C23H28O7
Mol Weight: 416.47
Botanical Source: Schisandra chinensis（Turcz.）Baill.
Physical Description:
Type of Compound: Lignans
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever 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 -20℃. Generally, these will be useable for up to two weeks.
The product could be supplied from milligrams to grams
Inquire for bulk scale.
Description:
Gomisin A has anti-inflammatory, antihypertensive, neuroprotective, and anti-proliferation properties, it induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. Gomisin A inhibits COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation.
References:
Int J Mol Med. 2013 Apr;31(4):888-98.
Protective effects of gomisin A isolated from Schisandra chinensis against CCl(4)-induced hepatic and renal injury.
The aim of the present study was to investigate the protective effects of Gomisin A, a lignan compound isolated from Schisandra chinensis, against liver and kidney damage induced by CCl(4) exposure.
METHODS AND RESULTS:
We assessed alterations in organ weights, levels of serum biochemical indicators, and activation of the caspase-3 and MAPK signaling pathways and carried out histological analysis of liver and kidney tissue in rats pretreated with Gomisin A for four days. In the Gomisin A/CCl(4)-treated group, only the liver experienced a significant increase in weight, whereas the other organs did not undergo any changes. Five biochemical indicators in serum indicated that liver and kidney toxicity dramatically decreased upon Gomisin A pretreatment, although the decrease in ratios varied. Upon histological analysis, the Gomisin A/CCl(4)-treated group showed less hepatocellular necrosis, a poorly dilated central vein in the liver section, decreased diameter of the glomerulus, a lower number of capillaries, and a convoluted tubule in the kidney section. Furthermore, the formation of active caspase-3 was inhibited by Gomisin A pretreatment in the Gomisin A/CCl(4)-treated group, whereas the expression level of Bax protein was slightly increased. Western blot analysis revealed that there were differences between the liver and kidney in terms of activation of the MAPK signaling pathway. In the liver, Gomisin A pretreatment increased phosphorylation of three members of the MAPK pathway when compared to that in the vehicle pretreatment group. However, in the kidney, only the phosphorylation level of p38 was elevated upon Gomisin A pretreatment, whereas levels of the other two members were decreased.
CONCLUSIONS:
These results suggest that Gomisin A induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway.
Biol Pharm Bull. 2012;35(11):1997-2003.
Gomisin A enhances tumor necrosis factor-α-induced G1 cell cycle arrest via signal transducer and activator of transcription 1-mediated phosphorylation of retinoblastoma protein.
Gomisin A, a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra chinensis, has been reported as an anti-cancer substance. In this study, we investigated the effects of Gomisin Aon cancer cell proliferation and cell cycle arrest in HeLa cells.
METHODS AND RESULTS:
Gomisin A significantly inhibited cell proliferation in a dose-dependent manner after 72 h treatment, especially in the presence of tumor necrosis factor-α (TNF-α), due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation. In addition, Gomisin A in combination with TNF-α strongly suppressed the expression of signal transducer and activator of transcription 1 (STAT1).
CONCLUSIONS:
Inhibition of STAT1 pathways by a small-interfering RNA against STAT1 and AG490 Janus kinase (JAK) kinase inhibitor AG490 reduced the cyclin D1 expression and RB phosphorylation, indicating that JAK-mediated STAT1 activation is involved in Gomisin A-induced G1 cell cycle arrest.
Biol Pharm Bull. 2012;35(2):171-7.
The molecular mechanisms of the hepatoprotective effect of gomisin A against oxidative stress and inflammatory response in rats with carbon tetrachloride-induced acute liver injury.
Oxidative damage and inflammation are implicated in the pathogenesis of liver injury and fibrosis. In the present study, we investigated the molecular mechanism by which Gomisin A conferred a hepatoprotective effect, focusing on its antioxidant and anti-inflammatory effects using rats with carbon tetrachloride (CCl(4))-induced acute liver injury.
METHODS AND RESULTS:
Pretreatment with Gomisin A prior to the administration of CCl(4) markedly prevented an increase in alanine aminotransferase, aspartate aminotransferase, and histological hepatic lesions. Gomisin A was also associated with a decrease in hepatic lipid peroxidation, and increased superoxide dismutase activity, suggesting that Gomisin A has an antioxidant effect. In addition Gomisin A treatment ameliorated mRNA levels of CCl(4)-induced inflammatory mediators, including tumor necrosis factor-α, interleukin-1β and inducible nitric oxide (NO) synthase, and the protein levels of transcriptional upregulator nuclear factor kappa B (NF-κB) and phospho-inhibitor of NF-κB (IκB). Furthermore, α-smooth muscle actin (α-SMA), a myofibroblast marker, was also inhibited by Gomisin A treatment.
CONCLUSIONS:
These results suggest that Gomisin A inhibits the oxidative stress and activation of NF-κB, leading to down-regulation of pro-inflammatory mediators and amelioration of fibrogenesis.
HPLC of Schizandrol B
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
Schizandrol B (CAS number: 58546-54-6) is a natural active diterpenoid compound isolated from Schisandra chinensis. Schisandra chinensis, as a traditional Chinese medicinal herb, has been widely studied and applied due to its diverse pharmacological effects. In recent years, as the incidence rate of neurodegenerative diseases continues to rise, searching for natural products with neuroprotective effects has become an important direction of drug research and development. Schisandrin B has gradually become a research hotspot due to its significant neuroprotective potential. This article aims to systematically review the chemical structure and physicochemical properties, plant sources and extraction methods, pharmacological activity, mechanism of action and molecular targets, pharmacological evaluation and pharmacokinetic characteristics of schisandrin B, and explore its clinical application prospects and future development directions.
The molecular formula of Schisandrin B is C24H-32O6, with a molecular weight of 416.4700. Its structure belongs to the class of bicyclic diterpenes, with multiple hydroxyl and methoxy substituents, giving it a relatively complex stereoisomeric configuration. Its LogP value is 3.0996, indicating that the molecule has moderate lipid solubility, which is beneficial for penetrating cell membranes and the blood-brain barrier. The TPSA (topological polar surface area) is 75.6100, indicating moderate polarity and a combination of hydrophilic and hydrophobic properties. The low water solubility (0.0052 mg/mL) to some extent limits its bioavailability, but its high blood-brain barrier permeability provides potential advantages for the treatment of neurological diseases. The negative result of hERG inhibition experiment indicates a low risk of cardiac toxicity. The Ames test result is 0.6, indicating a low risk of genotoxicity and meeting safety requirements.
Schisandrin B is mainly found in the fruit of Schisandra chinensis, which belongs to the Magnoliaceae family and is widely distributed in Northeast China, North China, and the Russian Far East. Traditionally, the fruit of Schisandra chinensis is used as medicine in a dry form, which has the effects of nourishing the liver and kidneys, nourishing the lungs and generating fluids.
The common methods for extracting schisandrin include solvent extraction, ultrasound assisted extraction, and high-performance liquid chromatography separation. Generally, ethanol or methanol is used as the extraction solvent to obtain high-purity schisandrin ethyl through a multi-step separation and purification process. In recent years, supercritical CO2 extraction technology has been introduced due to its green environmental protection and high selectivity, significantly improving extraction efficiency and purity. In addition, techniques such as column chromatography and reverse phase high-performance liquid chromatography (RP-HPLC) are commonly used for purification and quantitative analysis.
Schisandrin B exhibits significant pharmacological activity in various in vitro and in vivo models, particularly in the field of neuroprotection.
Neuroprotective effect
Schisandrin B can alleviate oxidative stress and inflammatory response, and protect neurons from damage. In Alzheimer's disease (AD) and Parkinson's disease (PD) models, schisandrin B improves cognitive function and motor disorders by regulating multiple signaling pathways. Its antioxidant activity is mainly achieved by activating the NRF2 signaling pathway, increasing intracellular expression of antioxidant enzymes, and reducing the accumulation of reactive oxygen species (ROS).
anti-inflammatory effect
Schisandrin B can inhibit the release of inflammatory mediators and reduce the level of neuroinflammation. By inhibiting the MAPK1 (ERK2) and NF - κ B signaling pathways, reducing the expression of pro-inflammatory cytokines such as TNF - α and IL-1 β, and alleviating the inflammatory response of the nervous system.
Anti apoptotic effect
This compound regulates the expression of BCL2 family proteins, inhibits CASP3 activation, prevents neuronal apoptosis, and protects neuronal cell survival.
Neurotransmitter regulation
Schisandrin ethyl has a certain inhibitory effect on acetylcholinesterase (ACHE), which may improve neurotransmitter balance, enhance neural signal transduction, and facilitate the recovery of cognitive function.
The neuroprotective effect of schisandrin B involves synergistic regulation of multiple targets and pathways, and the specific mechanism is as follows:
The comprehensive regulation of these molecular targets enables Schisandrin B to exhibit multidimensional therapeutic potential in the field of neuroprotection.
The pharmacological parameters of Schisandrin B indicate that it has good potential for drug development. The molecular weight of 416.47 conforms to Lipinski's rule, with a LogP of 3.0996, indicating moderate lipid solubility, which is beneficial for oral absorption and blood-brain barrier penetration. The TPSA is 75.61, indicating that its polarity is moderate and beneficial for cell membrane permeability.
Low water solubility (0.0052 mg/mL) is a major challenge for its drug development, which may affect its oral bioavailability. To address this issue, formulation techniques such as nanoparticle carriers and solid dispersions can be used to improve solubility and absorption rates.
The high permeability of the blood-brain barrier provides important advantages for the treatment of central nervous system diseases. HERG inhibits negative and low genotoxicity risks, indicating its good safety.
In terms of pharmacokinetics, existing studies have shown that Schisandrin B is rapidly absorbed after oral administration, with a moderate plasma half-life, mainly metabolized through the liver, and excreted mainly through bile and urine. Its high concentration in brain tissue supports its neuroprotective effect in vivo.
With the increasing number of patients with neurodegenerative diseases, it is urgent to develop safe and effective neuroprotective drugs. Schisandrin B has shown broad clinical application prospects due to its multi-target regulation and significant neuroprotective effects.
Future research should focus on the following aspects:
Preclinical safety and efficacy evaluation
Strengthen systematic toxicology research and multi animal model validation to clarify the safety and efficacy of long-term medication.
Formulation development and optimization of administration routes
Combining modern pharmaceutical technology to enhance water solubility and bioavailability, exploring various routes of oral, injection, and nasal administration.
In depth analysis of the mechanism
By utilizing multi omics and systems biology methods, we aim to further uncover its functional network and potential new targets, promoting the development of precise treatment strategies.
Clinical trial design
Gradually advance Phase I to III clinical trials to evaluate its efficacy and safety in Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases.
Combination therapy research
Explore synergistic effects with existing neuroprotective or anti-inflammatory drugs to enhance treatment efficacy and reduce adverse reactions.
Schisandrin ethyl, as an important active ingredient in Schisandra chinensis, has become a research hotspot in the field of natural product pharmacology due to its unique chemical structure and excellent neuroprotective activity. Its multi-target and multi pathway mechanism of action provides new ideas and potential drug candidates for the treatment of neurodegenerative diseases. Despite challenges such as low water solubility and limited bioavailability, modern formulation technology and in-depth mechanism research have the potential to overcome these bottlenecks and achieve clinical translation. In the future, Schisandrin B is expected to become an important drug in the field of neuroprotection, contributing to the improvement of patients' quality of life.
