4.7 Article

Schisandrin B attenuates epidural fibrosis in postlaminectomy rats by inhibiting proliferation and extracellular matrix production of fibroblasts

Journal

PHYTOTHERAPY RESEARCH
Volume 33, Issue 1, Pages 107-116

Publisher

WILEY
DOI: 10.1002/ptr.6204

Keywords

epidural fibrosis; fibroblast; MAPK; Schisandrin B; Smad2/3; TGF-beta 1

Funding

  1. Zhejiang Provincial Public Welfare Science and Technology Project [2017C33100]
  2. Zhejiang Public service technology research program/social development [LGF18H060008]
  3. Major scientific and technological project of medical and health of Zhejiang Province [WKJ-ZJ-1527]
  4. National Natural Science Foundation of China [81871806]

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Laminectomy has been widely considered one of the most common treatments for lumbar disorders. Epidural fibrosis (EF) is a common complication after laminectomy, causing recurrent postoperative pain. Schisandrin B (Sch.B), the active ingredient extracted from Schisandra chinensis Fructus, has been found to have potent antiproliferative and antifibrotic effects on several cells. This study aimed to investigate the effects of Sch.B on the prevention of postlaminectomy EF formation. In vitro, we studied the effects of Sch.B on transforming growth factor beta 1 (TGF-beta 1)-induced proliferation and extracellular matrix (ECM) production of primary fibroblasts, as well as its underlying mechanism. We found that Sch.B not only inhibited the proliferation of fibroblasts but also reduced ECM production, including that of connective tissue growth factor, fibronectin, and type I collagen, in a dose-dependent manner. Mechanistically, we found that Sch.B suppressed TGF-beta 1-stimulated activation of the Smad2/3 and mitogen-activated protein kinase pathways. Moreover, the in vivo study demonstrated that Sch.B treatment attenuated the progression of EF in a postlaminectomy rat model via reducing the cell number and ECM production of scar tissue. Taken together, these data suggested that Sch.B possesses great potential value as a preventative agent for EF.

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