Abstract
Ulcerative colitis (UC) is a chronic inflammatory disease with increasing incidence and prevalence in many countries. The purpose of this study is to explore the function of Schisandrin B and its underlying molecular mechanisms in colitis.In this study, mice with colitis were induced by giving 2.0% dextran sulfate sodium (DSS, MP) in the drinking water for seven days. Furthermore, TCMSP server and GEO DataSets were used to analyze the mechanism of Schisandrin B in colitis.It was found that Schisandrin B presented colitis in mice model. At the same time, Schisandrin B not only reduced inflammation in vivo and vitro model of colitis, but also suppressed the nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome in vivo and vitro model of colitis. In addition, Schisandrin B induced AMP-activated protein kinase (AMPK) / Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in model of colitis, and regulated AMPK protein at 316 sites. The inhibition of AMPK reduced the anti-inflammation effects of Schisandrin B on NLRP3 inflammasome. Apart from that, Schisandrin B decreased reactive oxygen species (ROS)-induced mitochondrial damage and reduced epithelial cells damage of colitis through regulating pyroptosis.Collectively, our novel findings for first time showed that, Schisandrin B suppressed NLRP3 inflammasome activation-mediated interleukin-1beta (IL-1β) level and pyroptosis in intestinal epithelial cells of colitis model through the activation of AMPK/Nrf2 dependent signaling-ROS-induced mitochondrial damage, which may be a significant therapeutic approach in the treatment of acute colitis.
Highlights
Ulcerative colitis (UC) is the inflammation of the rectal mucosa that usually extends proximally to other areas of the colon [1]
This study determined whether Schisandrin B reduced inflammation in vivo and vitro model of colitis
Schisandrin B suppressed NLRP3 expression and reduced mitochondrial damage in intestinal epithelial cells by LPS+ATP (Figure 3E). These results suggest that Schisandrin B suppressed NLRP3 inflammasome in vivo and vitro model of colitis, which may be attributed to mitochondrial damage
Summary
Ulcerative colitis (UC) is the inflammation of the rectal mucosa that usually extends proximally to other areas of the colon [1]. UC is characterized by cytokine imbalance, immune dysfunction and intestinal mucosa-associated inflammation [1]. UC patients generally present with bloody diarrhea, abdominal pain and tenesmus, with increasing global incidence [2]. There are approximately 286 cases per 100,000 people in the United States and 505 cases per 100,000 people in Europe [3]. There are limited data in developing countries. The incidence of UC is increasing year by year in Asia, Middle East and South America [4]
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