Yellow crystalline powder
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
466.6ºC at 760mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:4312-32-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
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. 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. 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.
Tetrahydrocoptisine Protects Rats From LPS-induced Acute Lung Injury
Weifeng Li 1 , Huimin Huang, Xiaofeng Niu, Ting Fan, Hua Hu, Yongmei Li, Huan Yao, Huani Li, Qingli Mu
Excessive alcohol consumption can lead to gastric ulcer and the present work was aimed to examine the protective effect of tetrahydrocoptisine (THC) in the model of ethanol-induced gastric ulcer in mice. Fasted mice treated with ethanol 75% (0.5ml/100g) were pre-treated with THC (10 or 20mg/kg, ip), cimetidine (100mg/kg, ip) or saline in different experimental sets for a period of 3days, and animals were euthanized 4h after ethanol ingestion. Gross and microscopic lesions, immunological and biochemical parameters were taken into consideration. The results showed that ethanol induced gastric damage, improving nitric oxide (NO) level, increased pro-inflammatory cytokine (TNF-α and IL-6) levels and myeloperoxidase (MPO) activity, as well as the expression of nuclear factor-κB (NF-κB) in the ethanol group. Pretreatment of THC at doses of 10 and 20mg/kg bodyweight significantly attenuated the gastric lesions as compared to the ethanol group. These results suggest that the gastroprotective activity of THC is attributed to reducing NO production and adjusting the pro-inflammatory cytokine, inhibited neutrophil accumulation and NF-κB expression.
COX-2; ELISA; GABAA; Gastric ulcer; IL-1; IL-1β; IL-6; MPO; Myeloperoxidase; NF-κB; NO; Nitric oxide; Nuclear factor-κB; PGE2; Pro-inflammatory cytokines; THC; TLRs; TNF; TNF-α; Tetrahydrocoptisine; The enzyme-linked immunosorbent assay; aminobutyric acid; cNOS; constitutive NO synthase; cyclooxygenase-2; iNOS; inducible NO synthase; interleukin (IL)-1β; interleukin-1; interleukin-6; myeloperoxidase; nitric oxide; nuclear factor kappa B; prostaglandin E2; tetrahydrocoptisine; toll-like receptors; tumor necrosis factor; tumor necrosis factor-alpha.
Protective Effect of Tetrahydrocoptisine Against Ethanol-Induced Gastric Ulcer in Mice
Weifeng Li 1 , Huimin Huang, Xiaofeng Niu, Ting Fan, Qingli Mu, Huani Li
2013 Oct 1
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)-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. 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.
Nitric oxide; Nuclear factor-kappa B; Phospho-ERK1/2; Phospho-p38MAPK; Pro-inflammatory cytokines; Tetrahydrocoptisine.
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
Weifeng Li 1 , Huimin Huang, Yanmin Zhang, Ting Fan, Xia Liu, Wei Xing, Xiaofeng Niu
2013 Sep 5