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Updated: Oct 12, 2025
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Published on: February 10, 2015
Schisandrin B regulates macrophage polarization and alleviates liver fibrosis via activation of PPARγ
Qingshan Chen1, Leilei Bao1, Lei Lv1
1Department of Pharmacy, Third Affiliated Hospital of Naval Military Medical University, Shanghai, China.
Background:
Schisandrin B (Sch B), the main ingredient of Schisandra chinensis, displays many bioactivities. This study aimed to identify the drug target of Sch B against liver fibrosis and describe the related molecular mechanisms.
Methods:
The effects of Sch B on liver fibrosis and macrophage polarization was investigated in vivo and in vitro. Furthermore, we analyzed the regulatory effect of Sch B on peroxisome proliferator-activated receptor gamma (PPARγ).
Results:
Our data showed that Sch B dramatically alleviated liver inflammation and fibrosis and inhibited macrophage activation via PPARγ. Sch B binds with PPARγ by molecular docking. Immunofluorescence double staining showed that PPARγ was mainly expressed in macrophages rather than hepatic stellate cells (HSCs) in liver fibrosis. Importantly, Sch B strongly inhibited macrophage polarization in fibrotic livers compared with the model group. Further, the results revealed that Sch B efficiently inhibited macrophage polarization and also decreased the levels of inflammatory cytokines in vitro. Knockdown of PPARγ by small interfering RNA (siRNA) inhibited the effect of Sch B on macrophage polarization. Mechanistically, Sch B regulated macrophage polarization through inhibition of the nuclear factor (NF)-κB signaling pathway via PPARγ both in vivo and in vitro.
Conclusions:
These results suggested that Sch B alleviated carbon tetrachloride (CCl4)-induced liver inflammation and fibrosis by inhibiting macrophage polarization via targeting PPARγ.
