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Dencichin (Dencichine)

Catalog No.GC31230

Dencichin is a non-protein amino acid originally extracted from Panax notoginseng, and can inhibit HIF-prolyl hydroxylase-2 (PHD-2) activity.

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Dencichin (Dencichine) Chemical Structure

Cas No.: 5302-45-4

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5mg
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10mg
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25mg
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Sample solution is provided at 25 µL, 10mM.

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Protocol

Cell experiment:

Cells are cultured in 6-well plates with glucose (LG) or high glucose control (HG) and then treated with valsartan (1.0 × 10-3 M) or Dencichin (1.0 × 10-5 M, 1.0 × 10-4 M and 1.0 × 10-3 M) for 24 h before analysing the activation of FN, Col I, and Col IV expression by ELISA and analysing MMP-9 and TIMP-1 expression by immunofluorescence. Each experiment is repeated at least three times throughout the study[2].

Animal experiment:

Male SD rats weighted approximately 200 ± 20 g (eight weeks old) are kept at 23 ± 2°C. The rats are randomLy allotted into two groups: normal group (n = 16) and diabetic nephropathy (DN) group (n = 60). The normal rats fed with normal diet and vehicle fall into the normal control group (NC, n = 8) and the normal rats fed with normal diet and Dencichin fall into the Dencichin control group (De C, n = 8). The rats in the diabetic group are fed the high-sugar-high-fat diet (composition: Common breeding material 54.6%, lard oil 16.9%, sucrose 14%, casein 10.2%, gunk 2.1%, maltodextrin 2.2%). Five weeks later, DN is induced by administering of 40 mg/kg STZ though intraperitoneal injection, and the normal rats are treated with vehiclecitrate buffer (0.1 M, pH 4.2). Next, the DN rats (n = 32) are assigned into four groups and oral administered with metformin hydrochloride (a positive control) at 80 mg/kg/day, (DN+Met, n = 8), which is dissolve into distilled water to make a 2 mg/mL solution before use; vehicle control for the DN control group (DN, n = 8), or Dencichin. The Dencichin group is divided into a high Dencichin group (160 mg/kg/day; DN+De H, n = 8) and a low Dencichin group (80 mg/kg/day; DN+De L, n = 8), which are dissolved into distilled water to make a 5 mg/mL and 2.5 mg/mL solution before use and oral administered at the dosage once per day. Blood glucose is measured each month. 8 w after administering with Dencichin, the rats are killed[2].

References:

[1]. Eslavath RK, et al. β-N-oxalyl-L-α, β- diaminopropionic acid induces HRE expression by inhibiting HIF-prolyl hydroxylase-2 in normoxic conditions. Eur J Pharmacol. 2016 Nov 15;791:405-411.
[2]. Jie L, et al. Dencichine ameliorates kidney injury in induced type II diabetic nephropathy via the TGF-β/Smad signalling pathway. Eur J Pharmacol. 2017 Oct 5;812:196-205.

Background

Dencichin is a non-protein amino acid originally extracted from Panax notoginseng, and can inhibit HIF-prolyl hydroxylase-2 (PHD-2) activity.

Dencichin (β-ODAP, 10 μM, 50 μM, 100 μM and 200 μM) increases HRE expression by 1.3±0.09, 2.5±0.07, 4.2±0.15 and 1.3±0.07 fold respectively compared to control. Dencichin has intermolecular interactions with PHD-2[1]. Dencichin (10 μM, 100 μM, 1 mM) significantly inhibits cell proliferation and extracellular matrix (ECM) proteins accumulation of HBZY-1 cells, and reduces the secretion of collagen I (Col I), collagen IV (Col IV), and fibronectin (FN)[2].

Dencichin improves metabolism disorder in diabetic nephropathy (DN) secondary to type II diabetes mellitus (DM) model. Dencichin (80, 160 mg/kg/day, p.o.) significantly prevents the up-regulation of TCH, TG, LDL, and HbAlc and the down-regulation of HDL in DN rats induced by STZ injection. Dencichin also attenuates renal injury induced in the DN secondary to type II DM model. Dencichin alleviates pancreas damage in the STZ-induced DN model. Dencichin regulates protein expression in the TGF-β/Smad signalling pathway in STZ-induced DN models[2].

[1]. Eslavath RK, et al. β-N-oxalyl-L-α, β- diaminopropionic acid induces HRE expression by inhibiting HIF-prolyl hydroxylase-2 in normoxic conditions. Eur J Pharmacol. 2016 Nov 15;791:405-411. [2]. Jie L, et al. Dencichine ameliorates kidney injury in induced type II diabetic nephropathy via the TGF-β/Smad signalling pathway. Eur J Pharmacol. 2017 Oct 5;812:196-205.

Chemical Properties

Cas No. 5302-45-4 SDF
Canonical SMILES N[C@@H](CNC(C(O)=O)=O)C(O)=O
Formula C5H8N2O5 M.Wt 176.13
Solubility Water: 5 mg/mL (28.39 mM); DMSO: 5 mg/mL (28.39 mM) Storage Store at -20°C
General tips Please select the appropriate solvent to prepare the stock solution according to the solubility of the product in different solvents; once the solution is prepared, please store it in separate packages to avoid product failure caused by repeated freezing and thawing.Storage method and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored at -20°C, please use it within 1 month.
To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time.
Shipping Condition Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request.
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Research Update

Biosynthesis of plant hemostatic dencichine in Escherichia coli

Dencichine is a plant-derived nature product that has found various pharmacological applications. Currently, its natural biosynthetic pathway is still elusive, posing challenge to its heterologous biosynthesis. In this work, we design artificial pathways through retro-biosynthesis approaches and achieve de novo production of dencichine. First, biosynthesis of the two direct precursors L-2, 3-diaminopropionate and oxalyl-CoA is achieved by screening and integrating microbial enzymes. Second, the solubility of dencichine synthase, which is the last and only plant-derived pathway enzyme, is significantly improved by introducing 28 synonymous rare codons into the codon-optimized gene to slow down its translation rate. Last, the metabolic network is systematically engineered to direct the carbon flux to dencichine production, and the final titer reaches 1.29 g L-1 with a yield of 0.28 g g-1 glycerol. This work lays the foundation for sustainable production of dencichine and represents an example of how synthetic biology can be harnessed to generate unnatural pathways to produce a desired molecule.

Dencichine prevents ovariectomy-induced bone loss and inhibits osteoclastogenesis by inhibiting RANKL-associated NF-κB and MAPK signaling pathways

Aims: To investigate the effect of dencichine on osteoclastogenesis in vivo and in vitro.
Methods: RANKL-induced osteoclastogenesis were treated with different concentrations of dencichine. Pit forming assays were applied to evaluate the degree of bone resorption. Osteoclastogenic markers were detected by real-time quantitative PCR (RT-qPCR) and Western blot. Micro CT was conducted to investigate the effects of dencichine on osteoclastogenesis in ovariectomized (OVX) mice.
Results: Dencichine suppressed osteoclastogenesis through the inhibition of phosphorylation of p65, p50 (NF-κB pathway), p38, ERK and JNK (MAPKs pathway) in vitro. Furthermore, dencichine inhibited the function of osteoclasts in a dose-dependent manner. In addition, the expression levels of the nuclear factor of activated T cells 1 (NFATc1) and osteoclastogenesis markers were decreased by dencichine, including MMP-9, Cathepsin K (CTSK), Tartrate-Resistant Acid Phosphatase (TRAP), C-FOS, dendritic cell specific transmembrane protein (DC-STAMP). In vivo data proved that dencichine alleviated ovariectomy-induced bone loss and osteoclastogenesis in mice.
Conclusion: Our results demonstrate that dencichine alleviates OVX-induced bone loss in mice and inhibits RANKL-mediated osteoclastogenesis via inhibition of NF-κB and MAPK pathways in vitro, suggesting that dencichine might serve as a promising candidate for treatment of bone loss diseases, including PMOP and rheumatoid arthritis.

Dencichine ameliorates renal injury by improving oxidative stress, apoptosis and fibrosis in diabetic rats

Objective: To investigate protective efficacies and mechanisms of dencichine on diabetic kidney injury via in vitro and in vivo assays.
Methods: Effects of dencichine on hydrogen peroxide (H2O2) induced oxidative damage in HK-2 renal cells were assessed by CCK-8 method. Forty streptozotocin (STZ)-induced diabetic rats with kidney injury were randomly divided into negative control group, three doses of dencichine (40, 80 and 160 mg/kg) groups. Blood biochemical and kidney related indexes as well adrenal morphological changes, apoptosis and autophagy related markers of diabetic rats were measured.
Results: Cell viability of HK-2 cells with oxidative damage induced by H2O2 was significantly improved by dencichine with 160 μg/mL for 43.7% and 320 μg/mL for 52.9% compared with control. Moreover, the decreased reactive oxygen species (ROS), and increased intracellular antioxidant enzymes including GPX1, SOD2 and GSH were showed in dencichine groups. In addition, incubation of dencichine in HK-2 cells promoted the increase of p-AMPK, BCL2, LC3, decreased activation of p-mTOR, BAX and Caspase 3. Chronic treatment of dencichine improved the STZ-induced diabetic characteristics of model rats. Further histopathological examination of renal tissues revealed 12-week treatment of dencichine effectively improved the morphology of nephropathy in diabetic rats. Moreover, dencichine also ameliorated excessive oxidation stress, down-regulated renal cell apoptosis and fibrosis related proteins, thereby protected renal tissues in diabetic rats.
Conclusion: Dencichine ameliorated STZ-induced kidney injury mainly through inhibiting oxidative stress, reducing renal fibrosis, increasing autophagy, and reducing the renal cell apoptosis related proteins to protect nephrocytes and decrease renal tissue damage.

Decichine enhances hemostasis of activated platelets via AMPA receptors

Introduction: Dencichine, one of the non-protein amino acids present in the roots of Panax notoginseng, has been found to shorten bleeding time of mice and increase the number of platelets. However, the exact underlying mechanisms have not been elucidated yet. This study was aimed to identify the hemostatic effect of dencichine and uncover its mechanisms.
Materials and methods: Hemostatic effect was assessed by measuring tail bleeding time and coagulation indices of rats. PT, APTT, TT and FIB concentration were measured using a Sysmex CA-1500 plasma coagulation analyzer. Platelet aggregation rate was determined by using a platelet aggregometer. Concentration of cyotosolic calcium was evaluated by Fluo-3 and levels of cyclic adenosine monophosphate (cAMP) and thromboxane A? (TXA?) were measured by ELISA method.
Results and conclusion: Dencichine administered orally shortened tail bleeding time, reduced APTT and TT but increased the concentration of FIB in plasma in a dose-dependent manner. When induced with trap, dencichine could elevate the cytoplasmic concentration of calcium, and secretion of TXA? as well as the ratio of TXA? to PGI? from platelets. Meanwhile, it decreased the level of intracellular cAMP. However, CNQX could block the enhanced hemostatic effect of dencichine. These results suggested that dencichine exerted hemostatic function via AMPA receptors on platelets, therefore, facilitated coagulation cascade in a paracrine fashion by control of platelet cytosolic calcium influx, cAMP production and TXA? release. Current study may contribute to its clinical use in therapy of hemorrhage.

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