Schisandrin B ameliorates high-glucose-induced vascular endothelial cells injury by regulating the Noxa/Hsp27/NF-κB signaling pathway

Background: To address the molecular mechanism of the anti-inflammation effects of schisandrin B (Sch B) in atherosclerosis, we examined injured HMEC-1, HBMEC, and HUVEC-12 cells induced by high glucose (HG). Methods: Western blot was performed to detect the levels of the proteins Hsp27, Noxa, TLR5, p-I kappa B alpha, and p-p65 in HG-induced cells, while ELISA was used to analyze the inflammatory cytokines TNF-alpha, IL-6, MCP-1, and IL-1 beta in cells with Hsp27 or Noxa stable expression. Results: Overexpression of Hsp27 upregulated the inflammatory cytokines and the release of I kappa B alpha, promoted transportation of p65 into the nucleus, and lastly, affected the inflammation process, while Sch B counteracted the upregulation. In addition, the effect of Noxa overexpression, which is different from Hsp27 overexpression, was consistent with that of Sch B treatment. Conclusions: Sch B may inhibit the inflammatory cascade and alleviate the injury to HMEC-1, HBMEC, and HUEVC-12 cells caused by HG by regulating the Noxa/Hsp27/NF-kappa B signaling pathway.