| In vivo: |
| Inflammation. 2014 Dec;37(6):2106-15. | | Tetrahydrocoptisine protects rats from LPS-induced acute lung injury.[Pubmed: 24928630] | Recent studies show that nuclear factor-kappa B (NF-κB) signaling pathway plays a key role in contributing to the development of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Tetrahydrocoptisine is one of the main active components of Chelidonium majus L. and has been described to be effective in suppressing inflammation. The aim of the present study is to evaluate the protective effect of Tetrahydrocoptisine on LPS-induced ALI in rats and clarify its underlying mechanisms of action.
METHODS AND RESULTS:
We found that in vivo pretreatment with Tetrahydrocoptisine to rats 30 min before inducing ALI by LPS markedly decreased the mortality rate, lung wet weight to dry weight ratio, and ameliorated lung pathological changes. Meanwhile, Tetrahydrocoptisine significantly inhibited the increase of the amounts of inflammatory cells, total protein content, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) secretion in the bronchoalveolar lavage fluids (BALFs). Furthermore, Tetrahydrocoptisine inhibited myeloperoxidase (MPO) accumulation in lung tissue and alleviated TNF-α and IL-6 production in serum. Additionally, immunohistochemistry showed that Tetrahydrocoptisine efficiently reduced nuclear factor-kappa B (NF-κB) activation by inhibiting the translocation of NF-κBp65.
CONCLUSIONS:
In conclusion, our results demonstrate that Tetrahydrocoptisine possesses a protective effect on LPS-induced ALI through inhibiting of NF-κB signaling pathways, which may involve the inhibition of pulmonary inflammatory process. | | Eur J Pharmacol. 2013 Sep 5;715(1-3):62-71. | | Anti-inflammatory effect of tetrahydrocoptisine from Corydalis impatiens is a function of possible inhibition of TNF-α, IL-6 and NO production in lipopolysaccharide-stimulated peritoneal macrophages through inhibiting NF-κB activation and MAPK pathway.[Pubmed: 23810685] | 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.
METHODS AND RESULTS:
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)-induced systemic inflammation model, THC significantly inhibited serum tumor necrosis factor-alpha (TNF-α) 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-α, interleukin-6(IL-6) and nitric oxide (NO) production. THC inhibited the production of TNF-α and IL-6 by down-regulating LPS-induced IL-6 and TNF-α 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(NF-κB), in a concentration-dependent manner.
CONCLUSIONS:
Taken together, our data suggest that THC is an active anti-inflammatory constituent by inhibition of TNF-α, IL-6 and NO production possibly via down-regulation of NF-κB activation, phospho-ERK1/2 and phospho-p38MAPK signal pathways. |
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