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. 2018 Apr 12;15(6):4599–4614. doi: 10.3892/etm.2018.6053

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Copyright: © Feng et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 9. — Sal ameliorates apoptosis and autophagy via activating the PI3K/Akt pathway in ConA-induced liver injury. In ConA-induced liver injury, the levels of IL-1β, IL-6 and TNF-α increase in the serum and liver tissues. Sal pretreatment reduces the production of these pro-inflammatory cytokines to relieve liver injury. Furthermore, Sal may activate the PI3K/Akt pathway to ameliorate liver injury. Following PI3K/Akt activation, Bad and Bax are phosphorylated and deactivated, and Bcl-2 is released from Bad, leading to the inhibition of apoptosis. Akt could also inhibit the production of caspase-9 to alleviate apoptosis. Released Bcl-2 conjugates with beclin-1 to form the Bcl-2/beclin-1 complex, interfering with the interaction between beclin-1 and VPS34, inhibiting the autophagy process. Thus, Sal successfully decreases liver injury in ConA-induced liver injury in mice. Sal, salidroside; ConA, concanavalin A; Bcl-2, B-cell lymphoma-2; Bax, Bcl-2-associated X protein; Bcl-2-associated death promoter; LC3, microtubule-associated protein 1A/1B-light chain 3; IL, interleukin; TNF-α, tumor necrosis factor-α; PI3K, phosphoinositide 3-kinase; mTOR, mechanistic target of rapamycin; VPS34, vesicular protein sorting 34.