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. 2015 Apr 9;9:2001–2027. doi: 10.2147/DDDT.S77071

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© 2015 Zhang et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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Proposed mechanisms for the cytotoxic effects of Sch B on mouse AML-12 and RAW 264.7 cells.

Notes: Sch B induces cell cycle arrest with up-regulation of the expression level of p27 Kip1 and Chk1, and down-regulation of the expression level of cyclin D1 and CDK2. Furthermore, Sch B induces the release of cytochrome c from mitochondria to cytosol, which promotes cleavage of caspase 3 and PARP, and leads to apoptosis. In addition, Sch B induces remarkable autophagy with the involvement of PI3K/Akt/mTOR signaling pathway in AML-12 and RAW 264.7 cells. The red ovals indicate key downstream targets of Sch B. The triangle means the balance of two key proteins.

Abbreviations: p, phosphorylated; Sch B, schisandrin B; PI3K, phosphatidylinositol 3-kinase; Akt, protein kinase B; mTOR, mammalian target of rapamycin; AMPK, 5′-adenosine monophosphate-activated protein kinase; LC3-I, cytosolic microtubule-associated protein 1A/1B-light chain 3; LC3-II, LC3-phosphatidylethanolamine conjugate; CDK, cyclin-dependent kinase; Chk1, checkpoint kinase 1; PARP, poly-adenosine diphosphate-ribose polymerase; Bcl-2, B-cell lymphoma 2; Bax, Bcl-2-like protein 4/Bcl-2-associated X protein.