| In Vitro |
Pinoresinol diglucoside (20-80 μM) inhibits RANKL-induced differentiation of RAW264.7 cells into osteoclasts[3].
Pinoresinol diglucoside (20-80 μM; 3 days) disrupts F-actin ring formation in RANKL-differentiated RAW264.7 osteoclasts, with complete disruption at 80 μM[3].
Pinoresinol diglucoside (20-80 μM; 3 days) inhibits the expression of osteoclast differentiation-related proteins NFATc1, c-Fos, CTSK, and TRAP in RANKL-differentiated RAW264.7 cells[3].
Pinoresinol diglucoside (20-80 μM; 3 days) inhibits activation of the NF-κB and AKT-GSK-3β signaling pathways in RANKL-treated RAW264.7 cells[3].
Pinoresinol diglucoside (80 μM) inhibits RANKL-induced nuclear translocation of p65 in RAW264.7 cells[3].
Pinoresinol Diglucoside alleviates oxLDL-induced dysfunction in human umbilical vein endothelial cells by restoring SOD activity, eNOS expression, and NO production[4].
Pinoresinol diglucoside (1 μM) attenuates hypoxia/reperfusion-induced injury in H9c2 cardiomyocytes by reducing oxidative stress, cell damage markers, and apoptosis, promoting cell viability, upregulating miR-142-3p, and downregulating HIF1AN[5].
Pinoresinol diglucoside (1 μM) has its protective effects against hypoxia/reperfusion-induced injury in H9c2 cardiomyocytes reversed by miR-142-3p overexpression, resulting in elevated oxidative stress, cell damage markers, and apoptosis, and reduced cell viability[5].
Pinoresinol diglucoside interacts strongly with zebrafish FZD2 and FZD5 in silico, with binding energies of -8.27 kcal/mol and -8.63 kcal/mol, respectively, indicating potential activation of Wnt signaling[6].
Pinoresinol Diglucoside (2.5-7.5 μg/mL; 24 h) inhibits high glucose-induced cardiac fibrotic responses in H9c2 cells by downregulating the TGF-β1/Smads signaling pathway[7].
Pinoresinol Diglucoside (2.5-7.5 μg/mL; 48 h) inhibits high glucose-induced EndMT in HUVECs[7].
Pinoresinol Diglucoside (2.5-7.5 μg/mL; 48 h) inhibits exogenous TGF-β1-induced EndMT in HUVECs[7].
The inhibitory effect of Pinoresinol Diglucoside (2.5-7.5 μg/mL; 48 h) on high glucose-induced EndMT in HUVECs is abolished by TGF-β1 knockdown, indicating PDG acts via the TGF-β1 pathway[7].
Pinoresinol diglucoside (25 μM; 24 h) preserves cell viability in HEI-OC1 cells, does not induce oxidative stress alone, and attenuates Cisplatin-induced oxidative stress and cell death in HEI-OC1 cells[9].
Pinoresinol diglucoside (25 μM; 24 h) downregulates SOCS1 protein expression in ex vivo neonatal mouse basilar membranes, and attenuates cCisplatin-induced SOCS1 upregulation in these membranes[9].
Pinoresinol Diglucoside (PDG) (2.5-7.5 μg/mL; 2 h pre-incubation, 24 h with ISO stimulation) inhibits isoproterenol-induced cardiac hypertrophy and inflammation in neonatal rat ventricular cardiomyocytes by reducing hypertrophic biomarker and pro-inflammatory cytokine mRNA expression[10].
Pinoresinol Diglucoside (PDG) (2.5-7.5 μg/mL; 24 h with PE stimulation) inhibits phenylephrine-induced activation of the AKT/mTOR/NF-κB signaling pathway in neonatal rat ventricular cardiomyocytes, reducing cardiac hypertrophy-associated protein expression[10].
Pinoresinol Diglucoside (2.5-7.5 μg/mL; 24 h) inhibits HG-induced fibrotic responses and downregulates the TGF-β1/Smads signaling pathway in H9c2 cells[12].
Pinoresinol Diglucoside (2.5-7.5 μg/mL; 48 h) inhibits HG-induced EndMT in HUVECs[12].
Pinoresinol diglucoside (0.1-1 μM; 60 min pre-incubation + 24 h co-treatment with oxLDL, or 24 h alone) inhibits oxLDL-induced apoptosis in HUVECs, with 1 μM completely abrogating the apoptotic effect and 0.1 μM reducing apoptotic cells to 17.2%[13].
Pinoresinol diglucoside (1 μM; 60 min pre-incubation + 24 h co-treatment with oxLDL, or 24 h alone) alleviates oxLDL-induced ROS and MDA production in HUVECs, reducing ROS levels by more than 20% compared to oxLDL-only treated cells[13].
Pinoresinol diglucoside (1 μM; 60 min pre-incubation + 24 h co-treatment with oxLDL, or 24 h alone) reverses oxLDL-induced inhibition of total SOD activity in HUVECs, restoring activity to near control levels[13].
Pinoresinol diglucoside (1 μM; 60 min pre-incubation + 24 h co-treatment with oxLDL, or 24 h alone) alleviates oxLDL-induced inhibition of NO production and eNOS mRNA expression in HUVECs, fully restoring both parameters to control levels[13].
Pinoresinol diglucoside (1 μM; 60 min pre-incubation + 24 h co-treatment with oxLDL, or 24 h alone) inhibits oxLDL-induced upregulation of LOX-1, ICAM-1, and NF-κB mRNA and protein expression in HUVECs, essentially abrogating the 1.7- to 3.5-fold upregulation caused by oxLDL[13].
Pinoresinol diglucoside (1 μM; 60 min pre-incubation + 45 min co-treatment with oxLDL, or 45 min alone) inhibits oxLDL-induced activation of the p38MAPK/NF-κB signaling pathway in HUVECs by reducing phosphorylation of p38MAPK and NF-κB p65[13].
Pinoresinol diglucoside (PG2) (1 μg/mL; 30 min at 38°C) inhibits β-glucuronidase activity by 80.0% in a cell-free anti-inflammatory assay[14].
Pinoresinol diglucoside (PG2) (1-1000 μM; 10 min) has an IC50 of 600 μM for DPPH radical scavenging activity in a cell-free assay, with activity increasing at higher concentrations[14].
Pinoresinol diglucoside (10 nM-10 μM; 3 days) at 1 μM maximally enhances osteogenic differentiation of neonatal mouse calvarial osteoblasts, as measured by ALP activity after 3 days of treatment[15].
Pinoresinol diglucoside (1 μM; 12-hour SMG exposure for proliferation, apoptosis, oxidative stress, cell cycle assays; 6 days of daily 12-hour SMG exposure for osteogenic differentiation assays) preserves osteogenic differentiation, reduces oxidative stress, enhances proliferation, inhibits apoptosis, and reverses G0/G1 cell cycle arrest in simulated microgravity-exposed neonatal mouse calvarial osteoblasts[15].
Pinoresinol diglucoside (1 μM; 3 days) maximally enhances alkaline phosphatase activity, a marker of osteogenic differentiation, in neonatal mouse calvarial osteoblasts[16].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Pinoresinol Diglucoside Related Antibodies
Western Blot Analysis[3]
| Cell Line: |
RANKL-differentiated RAW264.7 cells |
| Concentration: |
20 μM, 40 μM, 80 μM |
| Incubation Time: |
3 days |
| Result: |
Inhibited the expression of NFATc1, c-Fos, CTSK, and TRAP proteins significantly. |
Western Blot Analysis[3]
| Cell Line: |
RAW264.7 cells |
| Concentration: |
20 μM, 40 μM, 80 μM |
| Incubation Time: |
3 days |
| Result: |
Inhibited phosphorylation of IκBα, p65, AKT, and GSK-3β significantly, and inhibited degradation of IκBα. |
Cell Viability Assay[10]
| Cell Line: |
House Ear Institute-Organ of Corti 1 (HEI-OC1) |
| Concentration: |
25 μM; 30 μM (cisplatin, co-treatment) |
| Incubation Time: |
24 h |
| Result: |
Resulted in a 95.8% cell survival rate when used alone.
Resulted in a 91.7% cell survival rate when co-treated with 30 μM cisplatin.
Did not alter intracellular or mitochondrial reactive oxygen species (ROS) levels relative to control when used alone.
Markedly reduced cisplatin-induced increases in DCFH-DA (intracellular ROS) and MitoSOX (mitochondrial superoxide) fluorescence when co-treated with cisplatin.
Restored cisplatin-reduced mitochondrial membrane potential (JC-1 aggregate/monomer ratio) when co-treated with cisplatin. |
Apoptosis Analysis[13]
| Cell Line: |
human umbilical vein endothelial cells (HUVECs) |
| Concentration: |
0.1 μM (pre-incubated then co-treated with oxLDL); 1 μM (pre-incubated then co-treated with oxLDL); 1 μM (no oxLDL) |
| Incubation Time: |
60 min pre-incubation + 24 h co-treatment with oxLDL; 24 h (no oxLDL) |
| Result: |
Reduced oxLDL-induced HUVEC apoptosis from 25.7% to 17.2%.
Abrogated oxLDL-induced HUVEC apoptosis.
Did not induce apoptosis when administered alone. |
Western Blot Analysis[13]
| Cell Line: |
human umbilical vein endothelial cells (HUVECs) |
| Concentration: |
1 μM (pre-incubated then co-treated with oxLDL); 1 μM (no oxLDL) |
| Incubation Time: |
60 min pre-incubation + 45 min co-treatment with oxLDL; 45 min (no oxLDL) |
| Result: |
Significantly inhibited oxLDL-induced phosphorylation of p38MAPK and NF-κB p65 in HUVECs.
Did not affect p38MAPK or NF-κB p65 phosphorylation when administered alone. |
|
| In Vivo |
Pinoresinol diglucoside (10 mg/kg/day; p.o.; daily; 3 days) first undergoes deglycosylation to form metabolite M49, followed by in vivo metabolic reactions including furan-ring opening, demethoxylation, glucuronidation, and sulfation, and acts via 146 overlapping osteoporosis-related targets including BCL2, MARK3, GSK3B, HIF1A, ALB, and IL6 to modulate pathways including PI3K-Akt and estrogen signaling for potential anti-osteoporosis effects[1].
Pinoresinol diglucoside (5-10 mg/kg; i.v., caudal vein; single dose; 1 hour before MCAO induction) exerts dose-dependent neuroprotective effects against mouse MCAO/R-induced brain injury, and modulating anti-inflammatory and antioxidant pathways[2].
Pinoresinol Diglucoside (5-10 mg/kg; i.v. via caudal vein; single dose 1 h before MCAO) dose-dependently alleviates MCAO/R-induced brain injury in male C57BL/6 mice via inhibiting neuroinflammation through the NF-κB pathway and enhancing antioxidant activity through the Nrf2/HO-1 pathway, with the 10 mg/kg dose producing greater protective effects than the 5 mg/kg dose[4].
Pinoresinol Diglucoside (5-10 mg/kg; i.g.; daily; 3 weeks) significantly attenuates Aβ1-42-induced cognitive impairment, neuroinflammation, oxidative stress, and neuronal apoptosis in male BALB/c mice via modulation of the TLR4/NF-κB and Nrf2/HO-1 pathways[5].
Pinoresinol diglucoside (0.75-3 μM; exposure in culture medium; daily; 7 dpf to 9 dpf) mitigates dexamethasone-induced osteoporosis and chondrodysplasia in larval Danio rerio (zebrafish) by enhancing bone mineralization, correcting skeletal and cartilage malformations, improving motor function, upregulating osteogenesis-related genes, and activating Wnt signaling via interactions with FZD2 and FZD5 receptors[7].
Pinoresinol diglucoside (1-5 mg/kg/day; i.p.; daily; 8 weeks) dose-dependently alleviates DCM-induced cardiac fibrosis and endothelial-to-mesenchymal transition in db/db mice by downregulating the TGF-β1/Smads signaling pathway, with the 5 mg/kg/day high dose producing the most significant effects[8].
Pinoresinol diglucoside (25 mg/kg; i.p.; once daily; concurrent with Cisplatin dosing cycles) significantly attenuates Cisplatin-induced ototoxicity in male C57BL/6 mice by preserving cochlear hair cell survival, auditory function, and endocochlear potential, while inhibiting ferroptosis and NCOA4-mediated ferritinophagy via downregulation of SOCS1[10].
Pinoresinol Diglucoside (2.5-7.5 mg/kg per day; i.p.; daily; 3 weeks) dose-dependently attenuates AAC-induced cardiac hypertrophy in male Sprague Dawley rats, with the 7.5 mg/kg per day dose producing the most significant reduction in cardiac mass indices, hypertrophic biomarkers, fibrosis, inflammation, and activation of the AKT/mTOR/NF-κB signaling pathway[11].
Pinoresinol Diglucoside (7.5 mg/kg per day; i.p.; daily; 3 weeks) does not produce significant effects on cardiac structure, hypertrophic biomarkers, inflammation, or AKT/mTOR/NF-κB signaling in healthy male Sprague Dawley rats[11].
Pinoresinol diglucoside (1-5 mg/kg; i.p.; daily; 8 weeks) dose-dependently alleviates diabetic cardiomyopathy-induced cardiac fibrosis in db/db mice by inhibiting endothelial-mesenchymal transition via downregulation of the TGF-β1/Smads signaling pathway[12].
Pinoresinol Diglucoside (18-72 mg/kg; p.o.; daily; 21 days) effectively counteracts hindlimb unloading-induced bone loss in male C57BL/6J mice, with the 18 mg/kg oral daily dose for 21 days producing the greatest improvements in bone mechanical strength, mineral apposition rate, and markers of bone formation, resorption, oxidative stress, and inflammation[15].
Pinoresinol Diglucoside (18-72 mg/kg; p.o.; daily; 21 days) effectively counteracts hindlimb unloading-induced bone loss in male C57BL/6J mice, with the 18 mg/kg dose exhibiting optimal efficacy in restoring bone density, microstructure, mechanical strength, and bone metabolism balance[16].
Pinoresinol Diglucoside (30-100 mg/kg; i.v.; single dose) produces dose-dependent diastolic blood pressure reduction in anesthetized spontaneously hypertensive rats, with decreases ranging from 25 mmHg at 30 mg/kg to 120 mmHg at 100 mg/kg[17].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: |
Sprague-Dawley (male, 6-8 weeks old, 200-220 g)[1] |
| Dosage: |
10 mg/kg/day |
| Administration: |
p.o.; daily; 3 days |
| Result: |
Identified or tentatively characterized 51 metabolites across rat biological samples: 9 in plasma, 28 in urine, 13 in feces, 10 in liver, 4 in heart, 3 in spleen, 11 in kidneys, and 5 in lungs.
Identified 146 overlapping targets between pinoresinol diglucoside/its metabolites and osteoporosis, including BCL2, MARK3, GSK3B, HIF1A, ALB, and IL6.
Enriched key pathways including the PI3K-Akt signaling pathway, estrogen signaling pathway, MAPK signaling pathway, and Rap1 signaling pathway. |
| Animal Model: |
C57BL/6 (male, 7-8 weeks old, 20-23 g, middle cerebral artery occlusion/reperfusion model)[2] |
| Dosage: |
5 mg/kg; 10 mg/kg |
| Administration: |
i.v., caudal vein; single dose; 1 hour before MCAO induction |
| Result: |
Compared with the MCAO control group, the modified neurological severity score (mNSS) was significantly reduced, the infarct volume was significantly reduced to approximately 38%, brain water content was significantly reduced, and the number of intact neurons increased to approximately 40%.
Levels of TNF-α, IL-1β, IL-6, NO, ROS, and MDA in brain tissue were significantly decreased, while the activities of SOD, GSH, and GSH-Px were significantly increased.
Phosphorylation levels of IKKβ, IκBα, and p65 were significantly decreased, and p-p65 nuclear translocation was reduced.
Compared with the MCAO control group, the expression of NQO1, HO-1, and nuclear Nrf2 in brain tissue was significantly increased. |
| Animal Model: |
C57BL/6 (male, 7-8 weeks old, 20-23 g, middle cerebral artery occlusion/reperfusion model)[4] |
| Dosage: |
5 mg/kg; 10 mg/kg |
| Administration: |
i.v. via caudal vein; single dose 1 h before MCAO |
| Result: |
Significantly reduced neurological deficit scores, brain infarct volume, and brain water content compared to MCAO controls.
Improved neuronal morphological structure (reduced pyknotic nuclei, reversed apoptotic neuron morphology) and increased intact neuron count.
Significantly decreased brain tissue levels of TNF-α, IL-1β, IL-6, NO, ROS, and MDA.
Significantly increased brain tissue activities of SOD, GSH, and GSH-Px.
Significantly inhibited NF-κB pathway activation (reduced phosphorylation ratios of IKKβ and IkBα, reduced nuclear p-p65 levels).
Significantly increased brain tissue HO-1 and NQO1 protein expression, and increased nuclear Nrf2 levels.
Produced greater magnitude of protective effects (reduced neurological deficit scores, brain infarct volume, brain water content; improved neuronal structure; decreased pro-inflammatory/oxidative markers; increased antioxidant activities; inhibited NF-κB pathway; enhanced Nrf2/HO-1 pathway) at 10 mg/kg compared to 5 mg/kg. |
| Animal Model: |
BALB/c (male, 3 months old, 20-25g, stereotactic hippocampal injection of Aβ1-42)[5] |
| Dosage: |
5 mg/kg; 10 mg/kg |
| Administration: |
i.g.; daily; 3 weeks |
| Result: |
Reversed Aβ1-42-induced memory impairment, reducing escape latency in Morris water maze invisible platform trial, increasing percentage of time spent in target quadrant, and increasing number of target crossings.
Increased number of correct choices and reduced escape latency in Y-maze test.
Decreased brain tissue levels of proinflammatory cytokines TNF-α and IL-1β.
Reduced brain tissue levels of reactive oxygen species and malondialdehyde, and increased activity of antioxidant enzymes superoxide dismutase and catalase.
Upregulated the Bcl-2/Bax ratio, and downregulated expression of cleaved caspase-3 and cytochrome c in brain tissue, inhibiting neuronal apoptosis.
Reduced expression of TLR4 and activated NF-κB p65, and increased expression of Nrf2 and HO-1 in brain tissue.
All results were statistically significant (P < 0.05, P < 0.01, or P < 0.001 vs.
Aβ1-42 + vehicle group; n=10 per group). |
| Animal Model: |
db/db (8-week-old, 35-40g, spontaneous diabetic cardiomyopathy model); db/m (8-week-old, 18-20g, control)[8] |
| Dosage: |
1 mg/kg/day; 2.5 mg/kg/day; 5 mg/kg/day |
| Administration: |
i.p.; daily; 8 weeks |
| Result: |
Significantly inhibited collagen fiber deposition in cardiac interstitial and perivascular areas in a dose-dependent manner, with the high-dose group showing the greatest reduction in fibrosis area.
Reversed the upregulation of fibrotic marker mRNA levels (Col1a1, Col3a1, Postn) in a dose-dependent manner, with the high-dose group showing the most significant suppression.
Restored the mRNA levels of endothelial markers (CD31, Cdh5, Cldn5) and reduced the mRNA and protein levels of mesenchymal markers (α-SMA, FN1) in a dose-dependent manner.
Downregulated the protein expression of TGF-β1, p-Smad2, p-Smad3, and Smad4 in heart tissues in a dose-dependent manner. |
| Animal Model: |
C57BL/6 (male, 8-week-old)[10] |
| Dosage: |
25 mg/kg |
| Administration: |
i.p.; once daily; concurrent with cisplatin dosing cycles |
| Result: |
Mitigated cisplatin-induced increases in ABR hearing thresholds across 4, 8, 12, 16, 24, 32 kHz.
Significantly reduced cisplatin-induced elevations in DPOAE thresholds at 8, 12, 16, 24, 32 kHz, preserving outer hair cell function.
Increased cochlear hair cell counts per 100 μm in apex, middle, and base regions to levels matching or approaching control.
Reversed the >40% reduction in endocochlear potential (EP) caused by cisplatin, restoring EP values to near-control levels.
Downregulated cisplatin-induced overexpression of ferroptosis/ferritinophagy-related marker SOCS1 in cochlear tissue.
Reduced cisplatin-induced increases in NCOA4 protein expression while upregulating GPX4 and SLC7A11 protein expression.
Decreased cisplatin-induced co-localization of NCOA4 and LAMP1, and reduced cisplatin-induced autophagolysosome formation in cochlear cells. |
| Animal Model: |
Sprague Dawley (male, 8 weeks old, 180 g, partial abdominal aortic constriction-induced pressure overload)[12] |
| Dosage: |
2.5 mg/kg per day; 5 mg/kg per day; 7.5 mg/kg per day |
| Administration: |
i.p.; daily; 3 weeks |
| Result: |
Reduced heart weight/body weight ratio to 2.480 mg/g and left ventricular weight/heart weight ratio to 0.695 g/g (7.5 mg/kg dose, vs AAC vehicle group: 2.515 mg/g, 0.786 g/g).
Significantly reduced mRNA expression of hypertrophic biomarkers atrial natriuretic peptide and brain natriuretic peptide across all doses, with the most robust reduction at 7.5 mg/kg per day.
Reduced left ventricular collagen volume fraction and mRNA expression of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β across all doses compared to the AAC vehicle group.
Significantly inhibited AAC-induced increases in phosphorylated AKT, phosphorylated mTOR, and phosphorylated NF-κB p65 protein levels, while increasing IκB protein levels across all doses compared to the AAC vehicle group. |
| Animal Model: |
db/db (8-week-old, 35-40g, leptin receptor-deficient, spontaneous type 2 diabetes mellitus model with inherent cardiac fibrosis)[12] |
| Dosage: |
1 mg/kg; 2.5 mg/kg; 5 mg/kg |
| Administration: |
i.p.; daily; 8 weeks |
| Result: |
Significantly reduced interstitial and perivascular collagen fiber deposition in db/db mice, with a dose-dependent reduction in fibrosis area.
Dose-dependently reversed the elevated mRNA levels of fibrotic markers (Col1a1, Col3a1, Postn) in db/db mouse heart tissue.
Dose-dependently upregulated mRNA levels of endothelial markers (CD31, Cdh5, Cldn5) and downregulated mRNA levels of mesenchymal markers (α-SMA, FN1) in db/db mouse heart tissue, with corresponding changes in protein expression (α-SMA protein was dose-dependently reduced, and CD31 fluorescence intensity was dose-dependently increased via immunofluorescence).
Dose-dependently downregulated protein expression of TGF-β1, p-Smad2, p-Smad3, and Smad4 in db/db mouse heart tissue, with significant reductions in the ratios of TGF-β1/GAPDH, p-Smad2/t-Smad2, p-Smad3/t-Smad3, and Smad4/GAPDH observed at all doses, and the highest dose showing the strongest inhibitory effect. |
| Animal Model: |
C57BL/6J (male, 2 months old, 25-28 g, hindlimb unloading-induced osteoporosis model)[15] |
| Dosage: |
18 mg/kg; 36 mg/kg; 72 mg/kg |
| Administration: |
p.o.; daily; 21 days |
| Result: |
Reversed hindlimb unloading-induced reductions in femoral bone mineral density, trabecular bone volume fraction, trabecular bone mineral density, trabecular number, trabecular thickness, and cortical thickness, while decreasing trabecular separation relative to the untreated unloading group.
Significantly elevated mineral apposition rate compared to the untreated unloading group, with the 18 mg/kg dose showing the highest value.
Significantly increased maximum force and flexural strength relative to the untreated unloading group, with the 18 mg/kg dose showing the greatest improvement in flexural modulus.
At 18 mg/kg dose: Increased serum bone formation marker PINP, decreased serum bone resorption marker CTX-1, with levels not significantly different from normal control mice; significantly elevated femoral mRNA and protein levels of osteogenic markers Runx-2, OSX, and Col-I relative to the untreated unloading group; significantly increased the number of RUNX-2-positive cells on trabecular bone surfaces; significantly increased the number and area of ALP-stained bone marrow stromal cell colonies (CFU-F_ALP); significantly reduced the number of TUNEL-positive osteocytes in tibial cortical bone; significantly decreased serum levels of oxidative stress markers 8-isoPGF2α and 8-OHdG; significantly decreased serum levels of inflammatory cytokines IL-1β, IL-6, and TNF-α; significantly reduced femoral and serum RANKL/OPG ratios relative to the untreated unloading group. |
| Animal Model: |
Okamoto-Aobi strain spontaneous hypertensive rats (9-10 weeks old, 170-260 g, anesthetized)[17] |
| Dosage: |
30 mg/kg; 40 mg/kg; 100 mg/kg |
| Administration: |
i.v.; single dose |
| Result: |
Induced decreases in diastolic blood pressure of 25 mmHg and 35 mmHg in individual rats at 30 mg/kg.
Induced an 80 mmHg decrease in diastolic blood pressure at 40 mg/kg.
Induced decreases in diastolic blood pressure of 105 mmHg, 90 mmHg, 110 mmHg, and 120 mmHg in individual rats at 100 mg/kg.
Exhibited antihypertensive activity indistinguishable from the natural isolate from *Eucommia ulmoides*. |
|
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