Paeoniflorin inhibits lipopolysaccharide-induced inflammation in LO2 cells by regulating RhoA/NLRP3 pathway

• Main Authors: Haixia Liu, Fafeng, Cheng, Feifei Tang, Yifang Wang, Shuling Liu, Xueqian Wang
• Format: Article
• Language: English
• Published: Elsevier 2021-04-01
• Series: Journal of Traditional Chinese Medical Sciences
• Subjects: Paeoniflorin; Lipopolysaccharide; Inflammation; RhoA; NLRP3 inflammasome
• Online Access: http://www.sciencedirect.com/science/article/pii/S2095754821000429

Background: Inflammation is an essential component of liver diseases. Paeoniflorin (PF), a monoterpenoid component derived from peony root (Paeonia lactiflora Pall.), has anti-inflammatory, immunoregulatory, and hepatoprotective activities. However, whether PF affects liver inflammation and its underlying mechanisms is unclear. In this study, we investigated the effects of PF on lipopolysaccharide (LPS)-induced inflammation in LO2 cells and the underlying molecular mechanism. Methods: LPS was used to induce inflammation. After PF pretreatment for 2 h, the cells were treated with PF and LPS. Cell counting kit-8 was used to measure cell viability. Tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 were tested by Enzyme-linked immunosorbent assay. Western blot was used to evaluate TNF-α, Ras homolog family member A (RhoA), NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, and IL-1β proteins expression. Results: In LPS-induced LO2 cells, PF reduced TNF-α and IL-6 inflammatory cytokine production in a dose-dependent manner. LPS-induced TNF-α expression was also suppressed by PF. In addition, PF significantly inhibited LPS-induced RhoA activation (P = .0014). Finally, PF suppressed LPS-induced NLRP3 inflammasome activation by downregulating NLRP3, ASC, caspase-1, and IL-1β expression. Conclusion: These findings suggest that PF alleviates inflammation induced by LPS and further suggest the anti-inflammatory effect of PF may follow via reduced RhoA and NLRP3 inflammasome activity.