Anti-inflammatory effect of tetrahydrocoptisine from Corydalis impatiens is a function of possible inhibition of TNF-alpha, IL-6 and NO production in lipopolysaccharide-stimulated peritoneal macrophages through inhibiting NF-kappa B activation and MAPK pathway

作者：Li Weifeng; Huang Huimin; Zhang Yanmin; Fan Ting; Liu Xia; Xing Wei; Niu Xiaofeng^*

来源：European Journal of Pharmacology, 2013, 715(1-3): 62-71.

DOI：10.1016/j.ejphar.2013.06.017

• Tetrahydrocoptisine
• Nuclear factor-kappa B
• Pro-inflammatory cytokines
• Nitric oxide
• Phospho-ERK1/2
• Phospho-p3RMAPK

The extracts or constituents from Corydalis impatiens are known to have many pharmacological activities. Tetrahydrocoptisine (THC), a protoberberine compound from Corydalis impatiens, was found to possess a potent anti-inflammatory effect in different acute or chronic inflammation model animals. Pretreatment with THC (i.p.) inhibited the paw and ear edema in the carrageenan-induced paw edema assay and xylene-induced ear edema assay, respectively. In the lipopolysaccharide (LPS)-incluced systemic inflammation model, THC significantly inhibited serum tumor necrosis factor-alpha (TNF-alpha) release in mice. To clarify its possible molecular mechanisms underlying this anti-inflammatory effect, we investigated the effect of THC on LPS-induced responses in peritoneal macrophages. Our data demonstrated that THC significantly inhibited LPS-induced TNF-alpha interleukin-6(IL-6) and nitric oxide (NO) production. THC inhibited the production of TN-alpha and IL-6 by clown-regulating LPS-induced IL-6 and mRNA expression. Furthermore, it attenuated the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) and phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) as well as the expression of nuclear factor kappa B(INF-kappa B), in a concentration-dependent manner. Taken together, our data suggest that THC is an active anti-inflammatory constituent by inhibition of TNT-alpha, IL-6 and NO production possibly via clown-regulation of NF-K beta activation, phospho-ERK1/2 and phospho-p38MAPK signal pathways.

• 出版日期2013-9-5
• 单位西安交通大学