Liguzinediol
Liguzinediol is a Bcl-2 upregulator that exerts cardioprotective effects by upregulating Bcl-2, downregulating Bax and cleaved caspase-3, and inhibiting myocardial apoptosis, RAAS, oxidative stress, inflammation, and extracellular matrix remodeling. Liguzinediol can be used for research on heart failure and cardiac fibrosis.
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- CAS 番号: 909708-65-2
- 分子式: C8H12N2O2
- 分子量:168.20
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
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- 参考文献
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生物活性
製品説明
IC50 & Target
[1]|
Bax |
Bcl-2 |
Caspase-3 |
体外実験
Liguzinediol (10 μM) inhibits Ang II-stimulated cardiac fibroblast proliferation, ameliorates Ang II-stimulated morphological changes in cardiac fibroblasts, and reduces the ratio of type I/III collagen in Ang II-stimulated cardiac fibroblasts[2].
Liguzinediol (10 μM) downregulates MMP-2 and MMP-9 expression and upregulates TIMP-1 expression in Ang II-stimulated cardiac fibroblasts[2].
Liguzinediol (1-100 μM) produces a positive inotropic effect in isolated rat hearts without causing chronotropic changes[5].
Liguzinediol (100 μM) has no effect on the action potential duration of rat papillary muscle and left ventricular myocytes[5].
The positive inotropic effect of Liguzinediol (100 μM) is not mediated by β-AR, PDE, Na+-K+ ATPase, α1-AR, dopamine D1 receptor, or Na+-Ca2+ exchanger in isolated rat hearts[5].
Liguzinediol (100 μM) increases Ca2+ transients in rat left ventricular cardiomyocytes and restores caffeine-induced SR Ca2+ depletion[5].
Liguzinediol (100 μM) does not increase L-type Ca2+ channel current in rat left ventricular myocytes[5].
The positive inotropic effect of Liguzinediol (100 μM) is mediated by ryanodine receptor-dependent Ca2+ release in isolated rat hearts[5].
The positive inotropic effect of liguzinediol (100 μM) is mediated through SERCA2a-dependent Ca2+ handling in isolated rat hearts[5].
Liguzinediol (100 μM; 30 min) inhibits the activities of PP1 and PP2A in rat left ventricular tissue extracts, reducing PP1 activity to 86.0% of the control level and PP2A activity to 88.8% of the control level[6].
Liguzinediol (1-100 μM; 30 min) increases phosphorylation at PLB Ser-16 and Thr-17 sites in isolated rat ventricular myocytes in a concentration-dependent manner, reaching maximum ratios of 0.85 (p-PLB Ser-16/total PLB) and 0.35 (p-PLB Thr-17/total PLB) at 100 μM, respectively[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:rat ventricular myocytes
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Concentration:1, 10, 100 μM
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Incubation Time:30 min
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Result:Increased phosphorylation at PLB Ser-16 and Thr-17 sites in isolated rat ventricular myocytes in a concentration-dependent manner.
Parmacokinetics
体内実験
Liguzinediol (5-20 mg/kg; i.g.; once daily; two weeks) exerts protective effects against DOX-induced cardiac fibrosis in rats by reducing hydroxyproline content, decreasing the ratio of collagen type I/III, downregulating MMP-2 and MMP-9, and upregulating TIMP-1[2].
Liguzinediol (5-20 mg/kg; p.o.; daily; 8 weeks) alleviates myocardial infarction-induced heart failure in rats, and its protective effect is associated with the regulation of the TGF-β1/Smads pathway[3].
Liguzinediol (1-100 μM; retrograde coronary perfusion) produces a dose-dependent positive inotropic effect in isolated rat hearts, increasing LVDP to 187 mm Hg at 100 μM without changing heart rate[5].
Liguzinediol (20 mg/kg; intravenous injection; single administration) significantly increases left ventricular contractility in healthy male Sprague Dawley rats[6].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Sprague-Dawley (Male, 250 g, doxorubicin-induced cardiotoxicity)[1]
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Dosage:5, 10, 20 mg/kg/d
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Administration:p.o.; once daily; 2 weeks
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Result:Improved left ventricular systolic pressure (LVSP) to 110.47 mmHg and +LV dp/dtmax to 5693.05 mmHg/s at 10 mg/kg.
Improved LVSP to 122.80 mmHg and +LV dp/dtmax to 6502.72 mmHg/s at 20 mg/kg.
Showed -LV dp/dtmax of 4212.46 mmHg/s at 5 mg/kg.
Showed Bcl-2 protein content of 0.71, Bax protein content of 1.07, and Bax/Bcl-2 ratio of 1.52 at 10 mg/kg.
Showed pro-caspase-3 protein content of 0.94 and cleaved-caspase-3 protein content of 1.85 at 10 mg/kg.
Attenuated DOX-induced injury of cardiomyocytes, decreased the number of apoptotic bodies, and resulted in normal appearing nuclei, mitochondria with only minimal swelling, and normal appearing lamellar cristae at 10 mg/kg/d.
Weakened NF-κB staining and limited the number of myocardial fiber fractures and decreased the extent of inflammatory cell infiltration at 10 mg/kg.
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Animal Model:Sprague-Dawley rats (male, 250 ± 20 g, doxorubicin-induced cardiac fibrosis)[2]
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Dosage:5, 10, 20 mg/kg
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Administration:i.g.; once daily; two weeks
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Result:Improved myocardial fiber fracture, myocardial vacuolar degeneration, and inflammatory cell infiltration at 5 mg/kg.
Reduced breakage of myocardial fiber and vacuolar degeneration significantly at 10 mg/kg.
Showed a small amount of vacuolar degeneration at 20 mg/kg.
Led to a reduction in blue collagen fibers at 5 mg/kg.
Showed significantly less blue collagen fibers than the model group at 10 mg/kg.
Almost completely prevented the deposition of blue collagen at 20 mg/kg.
Decreased hydroxyproline content in a dose-dependent manner.
Decreased the ratio of type I/III collagen to 5.06 at 10 mg/kg.
Lowered MMP-2 protein abundance to 1.21 at 10 mg/kg.
Lowered MMP-9 protein content to 0.81 at 10 mg/kg.
Increased TIMP-1 protein content to 0.69 at 10 mg/kg.
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Animal Model:Sprague-Dawley (Male, 250-300 g, myocardial infarction-induced heart failure)[3]
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Dosage:5, 10, 20 mg/kg
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Administration:p.o.; daily; 8 weeks
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Result:Up-regulated EF and LVFS at 5, 10, 20 mg/kg.
Improved SV at 10, 20 mg/kg.
Inhibited the increase of LVEDs at 20 mg/kg.
Up-regulated LVSP, ±dp/dtmax, SBP, DBP and MAP, and down-regulated LVEDP at 5, 10, 20 mg/kg.
Reduced HMI and LVMI at 10, 20 mg/kg.
Reduced collagen deposition and myocardial fibrosis, reversed the increase of HYP, and reduced collagen I and III contents at 5, 10, 20 mg/kg.
Reduced IL-6 and TNF-α levels at 5, 10, 20 mg/kg.
Inhibited the increase of IL-1β at 10, 20 mg/kg.
Reversed the increase of MDA and increased SOD level at 5, 10, 20 mg/kg.
Reduced serum TGF-β, reversed increases of TGF-β1, p-Smad2, p-Smad3 and CD105, and promoted Smad7 expression at 5, 10, 20 mg/kg.
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Animal Model:Sprague-Dawley (SD) (male, 300-350 g)[5]
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Dosage:1 μM; 10 μM; 100 μM
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Administration:retrograde coronary perfusion
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Result:Increased LVDP from a control value of 102 mm Hg to 134 mm Hg (1 μM), 158 mm Hg (10 μM), and 187 mm Hg (100 μM) in a dose-dependent manner.
Increased +dp/dtmax from 2502 mm Hg/s (control) to 2773 mm Hg/s (1 μM), 3130 mm Hg/s (10 μM), and 3551 mm Hg/s (100 μM).
Increased −dp/dtmax from 1773 mm Hg/s (control) to 1957 mm Hg/s (1 μM), 2203 mm Hg/s (10 μM), and 2594 mm Hg/s (100 μM).
Did not alter heart rate across all doses (167 bpm, 169 bpm, and 160 bpm vs. control 163 bpm).
Upon washout, LVDP returned to 110 mm Hg, +dp/dtmax to 2683 mm Hg/s, and −dp/dtmax to 1843 mm Hg/s.
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Animal Model:Sprague-Dawley (SD) (male, 300-350 g)[5]
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Dosage:100 μM
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Administration:retrograde coronary perfusion
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Result:Nimodipine (1 μM) completely blocked the positive inotropic effect of LZDO (100 μM) on LVDP, with normalized values changing from 100% (control) to 98%.\nRuthenium red (5 μM) completely blocked the positive inotropic effect of LZDO (100 μM) on LVDP, with normalized values changing from 100% (control) to 97%.\nThapsigargin (2 μM), an irreversible SR Ca2+ ATPase inhibitor, completely blocked the positive inotropic effect of LZDO (100 μM) on LVDP, with normalized values changing from 100% (control) to 95%.\nNone of the tested antagonists or inhibitors (propranolol 1 μM, IBMX 5 μM, ouabain 1 μM, prazosin 1 μM, SCH23390 1 μM, KB-R7943 1 μM) blocked the enhancing effect of LZDO (100 μM) on LVDP in isolated rat hearts.
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Animal Model:Sprague Dawley (male, 300-350 g)[6]
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Dosage:20 mg/kg
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Administration:i.v.; single dose
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Result:Decreased end-systolic volume from 82 μL to 65 μL.
Increased end-systolic pressure from 115 mm Hg to 141 mm Hg.
Increased stroke volume from 116 μL to 136 μL.
Increased ejection fraction from 58.6% to 67.6%.
Increased cardiac output from 27066 μL/min to 31312 μL/min.
Increased peak rate of rise of left ventricular pressure (+dP/dtmax) from 7207 mm Hg/s to 10022 mm Hg/s (29.2% increase).
Increased stroke work from 10395 mm Hg/μL to 14988 mm Hg/μL.
Increased slope of end-systolic pressure-volume relationship (ESPVR) from 0.96 to 1.24 (29.2% increase).
Caused no significant changes in heart rate, end-diastolic volume, end-diastolic pressure, or slope of end-diastolic pressure-volume relationship.
- Collagen: Sirius Red Staining
- Annexin V plus membrane-impermeant dye apoptosis staining
- ROS/oxidative-stress fluorescent staining
- ECM-Embedded Organoid (Matrigel/Dome) Culture
- Connective Tissue: Masson's Trichrome/Collagen Trichrome Staining
- Research Protocol for Cardiovascular Diseases
- Research Protocol for Inflammation-related Diseases
- Matrigel Transwell/Boyden Chamber Invasion Assay
- Fibrosis/Collagen Morphometry
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Apoptosis Solutions
- Matrigel/ECM Transwell Invasion Assay
化学情報
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CAS 番号 909708-65-2
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分子量 168.20
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分子式 C8H12N2O2
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SMILES
OCC1=NC(=C(N=C1C)CO)C
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
[2]. Wu X, et al. Liguzinediol protects against cardiac fibrosis in rats in vivo and in vitro. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2016 May;80:260-267. [Content Brief]
[3]. Chen Q, et al. The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism. Chinese medicine. 2020;15:63. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
Liguzinediol 関連分類
HY-121864 関連分類
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