| In Vitro | In vitro activity: Schisandrin B is able to induce high level of apoptosis in human hepatic carcinoma cells and human leukemia cells. Schisandrin B decreases the viability of adenocarcinoma cells after UV exposure. The specific inhibitory effect of schisandrin B on ATR protein kinase activity (a DNA repair enzyme) following DNA damage in cells may be useful in anti-cancer therapy. Schisandrin B is found to be the only molecule being a cardioprotective agent as well as a dual inhibitor of P-glycoprotein and multidrug resistance-associated protein 1, which is potentially applicable to treat cancers, especially those displaying multidrug resistance
Cell Assay: 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. |
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| In Vivo | Schisandrin B can protect liver against toxicant challenge. Schisandrin B pretreatment protects against carbon tetrachloride- or TNFα-induced liver damage in mice. Further studies demonstrate the protective effect of schisandrin B on free radical-induced damage in various vital organs, including the heart, liver, kidney, brain and skin. Moreover, schisandrin B is found to attenuate cancer invasion and metastasis via inhibiting epithelial mesenchymal transition at the step of local invasion. |
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