Colorless columnar crystal
Schisandra chinensis,Eucommia ulmoides
Benzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxole, 5,6,7,8-tetrahydro-1,2,3,13-tetramethoxy-6,7-dimethyl-/GEMA-SCHIZANDRIN/1,2,3,13-Tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrobenzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxole/Schisandrin B
Methanol; Acetontrile; Ethyl Acetate; Acetone; Chloroform
545.0±50.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:61281-37-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Nature is a vast source of bioactive molecules and has provided an active and efficient reservoir for drug discovery. Among natural compounds, one of the most promising is Schisandrin B (Sch B), isolated from Schisandra chinensis, which was documented to possess diversified pharmacokinetic propriety, among them antioxidant, anti-inflammation, cardioprotection, and neuroprotection. Due to its large biological properties, Sch B was recorded to be a potent cure for several diseases by targeting several signaling pathways. This review is aimed at emphasizing the recent data on the biological properties of Sch B among the molecular mechanism of this drug on tumoral, cardiac, and neural diseases. The data suggest that the antitumor activities of Sch B were mainly through apoptosis and cell cycle arrest at the diver’s stage. It is reported that Sch B could be used as effective chemotherapy, neuroprotection, and cardioprotection since it possesses a spectrum of biological activities; however, further investigations on the mechanism of its action and preclinical trials are still mandatory to further validate the potential of this natural drug candidate.
Copyright © 2020 M. I. Nasser et al.
A Comprehensive Review on Schisandrin B and Its Biological Properties.
Nasser MI1, Zhu S1, Chen C1, Zhao M1, Huang H1, Zhu P1.
2020 Mar 14
Schisandrin B (Sch B) and miR-101 family members play critical roles in the pathogenesis of liver fibrosis. However, the relationship between them has not been reported yet. Thus, this study aims to fill this research gap. Results showed that Sch B significantly upregulated the expression of miR-101-5p in HSC-T6 cells. Sch B also increased the expression of miR-101-5p by combined administration of TGF-β1 and Sch B. Using miR-101-5p inhibitor, we demonstrated that Sch B can target miR-101-5p through the TGF-β signalling pathway to regulate the proliferation and activation of HSC-T6 cells. A rat model of carbon tetrachloride-induced liver fibrosis was established, and results indicated that Sch B can attenuate liver fibrosis by upregulating the expression of miR-101-5p. In conclusion, Sch B can directly target miR-101 to suppress liver fibrosis. Sch B or miR-101-5p may be used as a therapeutic approach for the prevention and treatment of liver fibrosis.
Schisandrin B; TGF-β signalling; liver fibrosis; miR-101-5p
Schisandrin B suppresses liver fibrosis in rats by targeting miR-101-5p through the TGF-β signaling pathway.
Cuiqiong W1, Chao X1, Xinling F1, Yinyan J1.
The natural medicinal monomer, schisandrin B (Sch B), has been shown to exert cardioprotective effects; however, the underlying mechanisms of these effects remain to be fully elucidated. Therefore, the aim of the present study was to investigate whether Sch B attenuated myocardial ischemia/reperfusion (I/R) injury via the phosphoinositide 3‑kinases (PI3K)/Akt signaling pathway. To confirm this, I/R models were established in rats by ligation of the left anterior descending coronary artery. A group of animals were administered with Sch B (60 mg/kg, lavage) and/or the PI3K inhibitor, LY294002 (0.3 mg/kg, intraperitoneal). Myocardial infarct size, myocardial infarct serum markers, myocardial apoptotic index and the expression of Akt were measured in each group. The results demonstrated that the administration of Sch B reduced the size of the myocardial infarct, and this effect was eliminated following LY294002 treatment. In addition, the administration of Sch B decreased the apoptotic index and the serum markers of myocardial infarction. Sch B administration also increased the expression of phosphorylated Akt, and Sch B treatment decreased the B‑cell lymphoma 2 (Bcl‑2)‑like protein 4/Bcl‑2 ratio and the expression of cleaved caspase‑3. Therefore, Sch B may protect myocardial tissue from I/R injury via the PI3K/Akt signaling pathway in rats.
Schisandrin B protects against myocardial ischemia/reperfusion injury via the PI3K/Akt pathway in rats.
Zhao X1, Xiang Y1, Cai C1, Zhou A1, Zhu N1, Zeng C1.
Schisandrin B(Wuweizisu-B) is a dibenzocyclooctadiene derivative isolated from Fructus Schisandrae, has been shown to produce antioxidant effect on rodent liver and heart.IC50 value:Target: in vitro: Schisandrin B exhibits anti-inflammatory activity through modulation of the redox-sensitive transcription factors Nrf2 and NF-κB. SB inhibited mitogen-induced proliferation and cytokine secretion by lymphocytes . Sch B can protect neuronal cells against oxidative challenge, presumably by functioning as a hormetic agent to sustain cellular redox homeostasis and mitoenergetic capacity in neuronal cells . Sch B exerted significant neuroprotective effects against microglial-mediated inflammatory injury in microglia-neuron co-cultures. Sch B significantly downregulated pro-inflammatory cytokines, including nitrite oxide (NO), tumor necrosis factor (TNF)-α, prostaglandin E(2) (PGE(2)), interleukin (IL)-1β and IL-6 . Sch B could inhibit TGF-β induced EMT of 4T1 cells and of primary human breast cancer cells .in vivo: Similar anti-inflammatory effects of SB on lymphocyte proliferation and cytokine secretion were also observed in vivo . Treatment with Sch B in CsA-treated mice significantly suppressed the elevation of blood urea nitrogen (BUN) and serum creatinine levels and attenuated the histopathological changes. Additionally, Sch B also decreased renal MDA levels and increased GSH levels in CsA-treated mice .