Tetrahydrocoptisine CAS NO.7461-02-1

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
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Chemical Properties of Tetrahydrocoptisine

Source of Tetrahydrocoptisine

The tubers of Corydalis yanhusuo

Biological Activity of Tetrahydrocoptisine

Protocol of Tetrahydrocoptisine

Preparing Stock Solutions of Tetrahydrocoptisine

References on Tetrahydrocoptisine

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-kappaB activation and MAPK pathway.[Pubmed:23810685]

Eur J Pharmacol. 2013 Sep 5;715(1-3):62-71.

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-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 TNF-alpha and IL-6 by down-regulating LPS-induced IL-6 and TNF-alpha 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-kappaB), in a concentration-dependent manner. Taken together, our data suggest that THC is an active anti-inflammatory constituent by inhibition of TNF-alpha, IL-6 and NO production possibly via down-regulation of NF-kappaB activation, phospho-ERK1/2 and phospho-p38MAPK signal pathways.

Tetrahydrocoptisine protects rats from LPS-induced acute lung injury.[Pubmed:24928630]

Inflammation. 2014 Dec;37(6):2106-15.

Recent studies show that nuclear factor-kappa B (NF-kappaB) 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-alpha (TNF-alpha) and interleukin-6 (IL-6) secretion in the bronchoalveolar lavage fluids (BALFs). Furthermore, Tetrahydrocoptisine inhibited myeloperoxidase (MPO) accumulation in lung tissue and alleviated TNF-alpha and IL-6 production in serum. Additionally, immunohistochemistry showed that Tetrahydrocoptisine efficiently reduced nuclear factor-kappa B (NF-kappaB) activation by inhibiting the translocation of NF-kappaBp65. In conclusion, our results demonstrate that Tetrahydrocoptisine possesses a protective effect on LPS-induced ALI through inhibiting of NF-kappaB signaling pathways, which may involve the inhibition of pulmonary inflammatory process.

[Synthesis and biological evaluation of tetrahydrocoptisine quaternary ammonium compounds].[Pubmed:23460970]

Yao Xue Xue Bao. 2012 Dec;47(12):1640-5.

The goal of treatment of metabolic syndrome is the prevention of diabetes and cardiovascular events. A series of novel Tetrahydrocoptisine quaternary ammonium compounds were prepared to evaluate their action of hypoglycemia and hypolipidemia for finding the therapeutic agents of metabolic syndrome. Starting from the coptisine hydrochloride (2), fifteen target compounds were synthesized by reduction and substitution of the 7-N position. All of the target compounds were characterized by 1H NMR and HR-MS. Their hypoglycemic activities were evaluated in HepG2 cell and hypolipidemic activities of compounds with better hypoglycemic activity were tested further in vivo. Results indicated that compounds 5, 7, 8 and 9 exhibited better hypoglycemic activities in vitro and compounds 5 and 8 exhibited good hypolipidemic activities in high-fat-diet (HFD) induced hyperlipidemia mice and (or) hamsters. However, the activity is not as good as simvastatin.

Protective effect of tetrahydrocoptisine against ethanol-induced gastric ulcer in mice.[Pubmed:23769714]

Toxicol Appl Pharmacol. 2013 Oct 1;272(1):21-9.

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-alpha and IL-6) levels and myeloperoxidase (MPO) activity, as well as the expression of nuclear factor-kappaB (NF-kappaB) 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-kappaB expression.

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