Schisandrin B attenuates bleomycin-induced pulmonary fibrosis in mice through the mTOR signaling pathway

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Qiaofa Lu
yang
zhou
Hu
Cai

Keywords

pulmonary fibrosis, bleomycin, autophagy

Abstract

Objectives: Schisandrin B (Sch B) is an active monomer of Schisandrin, which has anti-fibrosis pharmacological action. We examined whether Sch B could also alleviates bleomycin-induced (BLM-Induced) pulmonary fibrosis in mice and explored its anti-fibrosis mechanism.


Methods: We evaluated the effect of Sch B on BLM-Induced pulmonary fibrosis in mice. Histopathological examination was performed by H&E staining and immunohistochemistry. The inflammatory cytokines including IL-6 and TNF-α in serum and alveolar lavage fluid were determined by ELISA. Biomarkers of oxidative stress in lung tissues were measured by corresponding kits. Western blotting and immunofluorescence were used to investigate whether Sch B could regulate autophagy through the mTOR signaling pathway, in order to explore the possible molecular mechanism of Sch B attenuating pulmonary fibrosis.


Results: The results indicated that Sch B could significantly attenuate inflammation and oxidative stress, and inhibit pulmonary fibrosis in mice lungs. In addition, Sch B promoted autophagy to attenuate pulmonary fibrosis. The anti-fibrosis effect of Sch B was accomplished through the mTOR signaling pathway.


Conclusions: The results suggest that the anti-fibrotic effect of Sch B may be related to the activation of autophagy through the mTOR signaling pathway. Sch B may be a potential agent for the treatment of IPF.

Abstract 0 |

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