Dihydroparadol
Dihydroparadol is a iNOS inhibitor with an IC50 of 7.24 μM, and it is found in ginger. Dihydroparadol partially inhibits the catalytic activity of iNOS, blocks the nuclear translocation of NF-κB p65, reduces NF-κB activity, and attenuates lipopolysaccharide-induced degradation of IκB-α, thereby inhibiting NF-κB-mediated iNOS gene expression and protein production. Dihydroparadol inhibits lipopolysaccharide-induced nitric oxide production in macrophages and exhibits anti-inflammatory activity. Dihydroparadol increases ABCA1 protein abundance by elevating mRNA levels and reducing proteasomal degradation, and also increases ABCG1 protein abundance by enhancing protein stability. Dihydroparadol promotes cholesterol efflux from cholesterol-loaded macrophages via apolipoprotein A1-mediated and plasma-mediated pathways. Dihydroparadol inhibits PDGF-induced vascular smooth muscle cell proliferation, shows no cytotoxicity to vascular smooth muscle cells within the tested concentration range, and does not interfere with endothelial cell proliferation. Dihydroparadol can be used in the research of inflammatory diseases, atherosclerosis and cardiovascular diseases.
For research use only. We do not sell to patients.
- CAS No.: 143111-84-6
- Formula: C17H28O3
- Molecular Weight:280.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
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iNOS 7.24 μM (IC50) |
NF-κB |
IKK-α |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HCT-116 | IC50 |
82.2 μM
Compound: M9
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Cytotoxicity against human HCT116 cells assessed as growth inhibition after 24 hrs by MTT assay
Cytotoxicity against human HCT116 cells assessed as growth inhibition after 24 hrs by MTT assay
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[PMID: 22246389] |
| NCI-H1299 | IC50 |
77.7 μM
Compound: M9
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Cytotoxicity against human H1299 cells assessed as growth inhibition after 24 hrs by MTT assay
Cytotoxicity against human H1299 cells assessed as growth inhibition after 24 hrs by MTT assay
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[PMID: 22246389] |
In Vitro
Dihydroparadol (0.035-175 μM; 1 h pretreatment, followed by 20 h LPS stimulation) potently inhibits lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells with an IC50 of 7.24 μM, without reducing cell viability[1].
Dihydroparadol (0.35-17.5 μM; 1 h at 37°C) partially inhibits the catalytic activity of lipopolysaccharide-induced inducible nitric oxide synthase from RAW 264.7 murine macrophage cell homogenates, with inhibition plateauing at ~3.5 μM and a maximum inhibition of 14.8%[1].
Dihydroparadol (3.5-17.5 μM; 1 h pretreatment, followed by 20 h LPS stimulation) inhibits lipopolysaccharide-induced inducible nitric oxide synthase protein expression at 17.5 μM and enzyme activity with an IC50 of 0.88 μM in RAW 264.7 murine macrophage cells[1].
Dihydroparadol (0.35-17.5 μM; 1 h pretreatment, followed by 30 min LPS stimulation) inhibits lipopolysaccharide-induced IκB-α degradation in RAW 264.7 murine macrophage cells at concentrations of 3.5 μM and 17.5 μM[1].
Dihydroparadol (0.35-17.5 μM; 1 h pretreatment, followed by 30 min LPS stimulation) inhibits lipopolysaccharide-induced NF-κB p65 nuclear translocation in RAW 264.7 murine macrophage cells, with significant inhibition observed at concentrations of 3.5 μM and 17.5 μM[1].
Dihydroparadol (0.035-17.5 μM; 1 h pretreatment, followed by 4 h LPS stimulation) concentration-dependently inhibits lipopolysaccharide-induced NF-κB transcriptional activity in RAW 264.7 murine macrophage cells[1].
Dihydroparadol (rac-[5]-dihydroparadol) (30 min) inhibits PDGF-induced proliferation of primary rat aortic vascular smooth muscle cells with an IC50 of 10 μM[3].
Dihydroparadol (30 min) inhibits PDGF-induced proliferation of primary rat aortic vascular smooth muscle cells with an IC50 of 4.11 μM, as measured by crystal violet biomass staining[3].
Dihydroparadol (Up to 30 μM; 30 min) does not induce significant cytotoxicity in primary rat aortic vascular smooth muscle cells at concentrations up to 30 μM[3].
Dihydroparadol (Up to 30 μM; 48 h) does not interfere with the viability of human umbilical vein endothelial cells (HUVECtert) at concentrations up to 30 μM[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:RAW 264.7 murine macrophage cells
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Concentration:3.5-17.5 μM (iNOS protein expression); 0.035-100 μM (iNOS activity measurement)
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Incubation Time:1 h pretreatment, followed by 20 h LPS stimulation
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Result:Inhibited LPS-induced iNOS protein levels at 17.5 μM (but not 3.5 μM), confirmed by densitometric analysis.
Concentration-dependently inhibited LPS-induced iNOS enzyme activity with an IC50 of 0.88 μM.
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Cell Line:RAW 264.7 murine macrophage cells
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Concentration:0.35-17.5 μM
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Incubation Time:1 h pretreatment, followed by 30 min LPS stimulation
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Result:Significantly inhibited LPS-induced IκB-α degradation at 3.5 μM (94.6% of control) and 17.5 μM (130% of control).\nIncreased cytoplasmic NF-κB p65 levels to 79.7% of control and reduced nuclear NF-κB p65 levels to 69.8% of LPS-stimulated control at 3.5 μM.
Reduced nuclear NF-κB p65 levels to 37.8% of LPS-stimulated control at 17.5 μM, a level comparable to positive control PDTC.
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Cell Line:Primary rat aortic vascular smooth muscle cells (VSMC)
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Concentration:Up to 30 μM
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Incubation Time:30 min h (post-PDGF stimulation)
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Result:Showed no significant cytotoxicity toward VSMC, as measured by LDH release, at concentrations up to 30 μM.
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Cell Line:Human umbilical vein endothelial cells (HUVECtert)
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Concentration:Up to 30 μM
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Incubation Time:30 min h
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Result:Showed no significant negative effect on HUVECtert viability at concentrations up to 30 μM.
Chemical Information
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CAS No. 143111-84-6
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Molecular Weight 280.40
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Formula C17H28O3
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SMILES
OC1=CC=C(CCC(CCCCCCC)O)C=C1OC
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Somatic Cell Culture
A method of simulating the in vivo environment in vitro to maintain the cell growth, differentation and main functions.
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Cytoplasmic-Nuclear Fractionated Protein Extraction
Cytoplasmic-nuclear fractionated protein extraction separates soluble cytoplasmic proteins from nuclear-enriched proteins by mild plasma-membrane permeabilization, differential centrifugation, washing of nuclei, and extraction of nuclear proteins for downstream immunoblotting or related molecular analysis. The readout is the relative abundance of a protein in cytoplasmic and nuclear fractions, commonly assessed by western blotting together with compartment markers such as tubulin or pyruvate kinase for cytoplasm and lamin, nucleoporin, hnRNP, H2AX, or Lamin B for nuclear fractions.
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
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RT-PCR
Reverse transcription technology uses RNA as a template to synthesize DNA. RT-PCR is simple, specific and sensitive, and can be used to detect gene expression levels and expression differences in cells; detect RNA virus content; clone cDNA sequences of specific genes.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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BrdU Incorporation Assay
Bromodeoxyuridine (BrdU) incorporation assay is based on the principle that BrdU, a thymidine analog, is incorporated into newly synthesized DNA during the S phase of the cell cycle, thereby serving as a marker of DNA replication and cellular proliferation. Incorporated BrdU can be detected using anti-BrdU antibodies following DNA denaturation, enabling visualization or quantification of proliferating cells through immunochemical detection methods such as immunofluorescence or immunohistochemistry.
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CFSE Dye Dilution Proliferation Assay
The CFSE (carboxyfluorescein diacetate succinimidyl ester) dye dilution proliferation assay is based on the covalent labeling of intracellular proteins by a cell-permeant fluorescent dye that becomes fluorescent upon intracellular ester cleavage and then is stably retained within cells. As labeled cells divide, the dye is partitioned equally between daughter cells, resulting in a stepwise halving of fluorescence intensity that can be quantified by flow cytometry to determine the number of cell divisions undergone by each cell population. This fluorescence dilution approach enables quantitative tracking of lymphocyte proliferation at the single-cell level over multiple rounds of division. CFSE-based proliferation analysis has been widely applied to measure antigen-driven lymphocyte expansion in vitro, where discrete fluorescence peaks correspond to successive cell divisions and allow reconstruction of proliferative history within heterogeneous populations.
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Dye-dilution cell tracking and proliferation staining
Dye-dilution cell tracking assays quantify cell proliferation by covalently labeling intracellular proteins with a stable fluorescent dye that is equally partitioned between daughter cells during mitosis, resulting in stepwise halving of fluorescence intensity with each cell division as measured by flow cytometry histograms. Carboxyfluorescein diacetate succinimidyl ester (CFSE) is a prototypical dye that diffuses into cells, is enzymatically converted into a fluorescent compound, and then covalently binds intracellular amine groups, producing long-lived fluorescence suitable for tracking multiple rounds of division in vitro and in vivo. Successive generations of dividing cells form discrete peaks of decreasing fluorescence intensity, enabling estimation of proliferation history, precursor frequency, and division index within heterogeneous populations. Alternative dyes such as CellTrace Violet (CTV) and far-red membrane dyes (e. g. , PKH26) follow the same dilution principle but differ
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CCK-8/WST-8 Cell Proliferation Assay
The CCK-8/WST-8 assay is based on the reduction of the water-soluble tetrazolium salt WST-8 to a water-soluble formazan product by cellular dehydrogenases in metabolically active cells, where the generated formazan amount is proportional to the number of living cells and is quantified by measuring absorbance in the visible range, providing a colorimetric readout for cell viability and proliferation assessment. This class of tetrazolium-based assays improves upon earlier MTT-based systems by producing a water-soluble formazan, eliminating the need for organic solubilization steps and enabling direct spectrophotometric measurement in culture medium.
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Protocol for Cell Cycle
Cell-cycle analysis by flow cytometry measures DNA content in single cells to estimate the fraction of cells in G0/G1, S, and G2/M phases. Propidium iodide intercalates into DNA, and after RNA removal with RNase, fluorescence intensity reflects cellular DNA content: 2N cells are assigned to G0/G1, cells between 2N and 4N to S phase, and 4N cells to G2/M. DNA-content analysis alone cannot reliably separate G0 from G1 or G2 from M. Ki-67 can distinguish quiescent G0 cells from cycling cells, EdU or BrdU incorporation marks active DNA synthesis in S phase, and phospho-histone H3 staining identifies mitotic cells within the 4N population.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Cell Counting-Based Growth Curve Assay
Cell counting-based growth curve assays quantify cell proliferation by directly measuring changes in viable cell number over time using manual or automated counting methods such as hemocytometer-based counting or instrument-assisted cell enumeration, enabling construction of growth curves that reflect population expansion dynamics in response to culture conditions. A widely used approach is trypan blue exclusion with hemocytometer counting, where membrane-compromised (non-viable) cells take up the dye, allowing discrimination between viable and non-viable cells while simultaneously enabling total cell number quantification. Repeated sampling across time points allows estimation of proliferation rate, growth phases, and comparative growth kinetics between experimental conditions.
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Colony Formation (Clonogenic) Assay
The clonogenic (colony formation) assay measures the ability of a single cell to retain reproductive viability and form a macroscopic colony, typically defined as a cluster derived from one progenitor cell after a defined growth period. This assay is widely used to evaluate cell survival after exposure to ionizing radiation or cytotoxic treatments and is considered a standard method in radiation biology for generating dose-response relationships of reproductive cell death. Colony formation reflects long-term proliferative capacity rather than short-term metabolic activity, and survival is quantified by comparing treated versus untreated conditions based on colony number and derived survival fractions.
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Real Time qPCR (Q-PCR)
Real-time quantitative PCR (qPCR) quantifies an amplifiable nucleic-acid target by monitoring fluorescence during PCR cycling rather than measuring product only after amplification. The increase in fluorescence tracks accumulation of PCR product, and the quantification cycle (Cq; historically also Ct/CP) is related to the initial amount of target: samples containing more starting target generally reach the defined fluorescence threshold in fewer cycles.
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Protocol For Protein Expression And Purification
Recombinant protein expression in Escherichia coli followed by purification of a His-tagged soluble protein by immobilized metal affinity chromatography (IMAC), with optional MBP fusion and TEV tag removal when the construct includes these elements. The biological readout is production of the encoded target protein, detected as an inducible band at the expected molecular mass by SDS-PAGE and quantified by total protein assay or chromatographic absorbance; the purification readout is enrichment of the target protein in elution fractions after selective binding of polyhistidine residues to immobilized Ni2+/metal-chelate resin and elution by imidazole-containing buffer. Expression is driven by an inducible bacterial expression system, commonly T7/lac-based, in which IPTG or lactose/auto-induction activates transcription and translation of the cloned gene; lower induction temperature, lower inducer concentration, induction timing, and solubility-enhancing fusion tags can influence the frac
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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EdU Incorporation Assay (Click Chemistry-Based DNA Synthesis Measurement)
The EdU incorporation assay measures DNA synthesis by adding the thymidine analog 5-ethynyl-2′-deoxyuridine to cells or tissues, where it is incorporated into newly synthesized DNA during S phase. Incorporated EdU is detected by copper-catalyzed azide-alkyne cycloaddition, in which a fluorescent azide covalently reacts with the ethynyl group on EdU, allowing S-phase cells to be detected by fluorescence microscopy, flow cytometry, or high-content imaging. EdU detection does not require DNA denaturation or anti-BrdU antibody access, which preserves sample structure and improves compatibility with immunostaining and multiparameter cytometry compared with BrdU-based detection. EdU can be cytotoxic in a cell-type- and exposure-dependent manner, so pulse duration, concentration, and continuous-labeling designs should be validated for each cell type.
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Ki-67 Immunostaining Proliferation Assay
Ki-67 immunostaining measures the growth fraction of a cell population by detecting Ki-67, a nuclear antigen present in proliferating cells and absent in quiescent G0 cells. The readout is the percentage of Ki-67-positive nuclei among total counted cells, commonly called the Ki-67 labeling index or proliferation index.
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PCNA Immunodetection Proliferation Assay
PCNA immunodetection measures proliferative activity by detecting proliferating cell nuclear antigen, a nuclear protein associated with DNA polymerase δ function and DNA replication. The assay readout is the proportion of PCNA-positive nuclei among total counted cells, but PCNA labeling is not identical to BrdU labeling because PCNA can mark late G1/early S-associated replication competence and may persist beyond active DNA synthesis depending on fixation and extraction conditions.
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Cotton Pellet Granuloma
Cotton pellet granuloma is a classical in vivo chronic inflammation model used to evaluate the anti-inflammatory potential of test substances by measuring their ability to inhibit granuloma tissue formation around an implanted foreign body (cotton pellet) in rodents. The method is based on the biological response to a sterile implanted material, which induces proliferative phase inflammation characterized by fibroblast proliferation and collagen-rich granuloma formation, and the final readout reflects the extent of chronic inflammatory tissue growth surrounding the pellet. In multiple preclinical pharmacological evaluations, inhibition of cotton pellet-induced granuloma formation has been used as an indicator of anti-inflammatory activity in both synthetic and natural product screening contexts.
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Protocol for Cell Counting and Cell Density Analysis
Cell counting and cell-density analysis estimate the number of cells in a known volume or field area. Manual hemocytometer counting uses a chamber of defined geometry to convert counted cells into cells/mL, while automated counters and image-analysis workflows detect cell objects from optical, brightfield, fluorescence, impedance, or digital-image features. Trypan blue viability counting is based on dye exclusion: viable cells with intact membranes exclude dye, while non-viable cells with compromised membranes stain blue. The readout is total cell density, viable-cell density, dead-cell density, and percent viability. Cell density can also be estimated from microscopy images by counting objects per image area, from flow cytometry using calibrated volume or reference particles, or from in situ microscopy in bioreactors after calibration against reference methods such as hemocytometer or flow cytometry.
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Carrageenan-Induced Paw Edema
Carrageenan-induced paw edema is an acute inflammation model in which intraplantar injection of carrageenan induces localized inflammatory swelling characterized by vascular permeability, leukocyte infiltration, and production of inflammatory mediators such as prostaglandins and cytokines, making it widely used to evaluate anti-inflammatory agents in vivo. The resulting paw volume or thickness increase is quantified over time as a direct readout of inflammatory intensity and drug efficacy, typically reflecting cyclooxygenase-mediated prostaglandin-driven edema formation and immune cell recruitment in peripheral tissue[20].
Purity & Documentation
References
[1]. Aktan F, et al. Gingerol metabolite and a synthetic analogue Capsarol inhibit macrophage NF-kappaB-mediated iNOS gene expression and enzyme activity. Planta medica. 2006 Jun;72(8):727-34. [Content Brief]
[2]. Wang D, et al. 6-Dihydroparadol, a Ginger Constituent, Enhances Cholesterol Efflux from THP-1-Derived Macrophages. Molecular nutrition & food research. 2018 Jul;62(14):e1800011. [Content Brief]
[3]. Liu R, et al. Identification and characterization of [6]-shogaol from ginger as inhibitor of vascular smooth muscle cell proliferation. Molecular nutrition & food research. 2015 May;59(5):843-52. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)