Biological Activity

Bioactivity / Mechanism

In cisplatin-exposed HEI-OC1 cells, pinoresinol diglucoside was associated with lower oxidative and labile-iron signals, reduced NCOA4/LAMP1 colocalization and fewer autolysosomes. These findings support a ferroptosis/ferritinophagy-associated cellular phenotype; they do not establish direct binding to NCOA4 or SOCS1. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

In Vitro Studies

HEI-OC1 cells co-exposed to pinoresinol diglucoside (25 µM) and cisplatin (30 µM) for 24 h showed higher survival and lower ROS and mitochondrial injury readouts than cells exposed to cisplatin alone. Live/dead staining yielded text-reported survival of 91.7% with co-treatment versus 45.6% with cisplatin alone. Untreated and PDG-only controls were included. [1]

Protection against cisplatin-associated injury in HEI-OC1 cells

Cell-based study · House Ear Institute-Organ of Corti 1 (HEI-OC1) cells; untreated, cisplatin-only, PDG-only and PDG + cisplatin groups [1]

A 24 h co-exposure design showed a higher live-cell fraction and lower oxidative/iron-associated injury readouts in the PDG + cisplatin group than in the cisplatin-only group. Survival and redox/morphology endpoints are retained together as one treatment design. The experiments do not demonstrate direct molecular binding or clinical otoprotection; explicit solvent matching is not documented.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Live-cell fraction after cisplatin exposure, with or without PDG	reported cell survival Cisplatin: 45.6%; PDG alone: 95.8%; PDG + cisplatin: 91.7%. These are text-reported point values, not fitted IC50 values.	[1]
Intracellular and mitochondrial ROS and mitochondrial membrane potential	direction versus cisplatin alone PDG + cisplatin reduced DCFH-DA and MitoSOX signals and partially restored the JC-1 aggregate/monomer readout; PDG alone had no significant effect versus control in the displayed comparisons.	[1]
Lipid peroxidation and cellular/mitochondrial ferrous iron	direction versus cisplatin alone PDG + cisplatin reduced MDA and labile iron readouts and attenuated the BDP lipid-oxidation response.	[1]
NCOA4/LAMP1 colocalization and autolysosome counts	direction versus cisplatin alone PDG + cisplatin showed reduced NCOA4/LAMP1 colocalization and fewer autolysosomes. These are cellular association readouts, not a PDG–protein binding assay.	[1]

Literature-Reported Treatment Conditions

Treatment concentration: 25 µM PDG
Exposure duration: 24 h
Method: Co-culture with cisplatin for the injury condition; no pretreatment interval assumed.
Vehicle: PDG stock: 50 mM in DMSO; cisplatin stock: 3 mM in sterile PBS.
Co-treatment: 30 µM cisplatin for 24 h in the injury and co-treatment groups; PDG-only and untreated groups included.
Reported limits: Final solvent fractions, explicit vehicle matching, paper-specific lot/purity/stereochemical analysis and the biological unit behind each panel n are not specified in the read assay text. Methods report at least three independent experiments; panel n is preserved without assuming it counts independent cell preparations.

Methods and source locations

Compound reported in the paper: Pinoresinol diglucoside; Compound label in the paper: PDG; MCE HY-N0657

Reported effects of the named supplier reagent in this cellular model; not a statement that Adooq material was tested.

Results 2.1–2.2; Figures 1A–I and 2A–J; Experimental Section: Cell Culture and Drug Treatments, Cell Viability Assay, ROS Detection, Lipid Peroxidation Detection, Ferrous Ion Detection, Immunofluorescence Staining, Transmission Electron Microscopy, Statistical Analysis

Live-cell fraction after cisplatin exposure, with or without PDG: Calcein-AM/propidium iodide live/dead staining; Figure 1A–B n = 4; mean ± SD shown graphically, numerical SD not supplied in the Results text. — Results 2.1; Figure 1A–B and caption; Cell Viability Assay

Intracellular and mitochondrial ROS and mitochondrial membrane potential: DCFH-DA, MitoSOX and JC-1 microscopy, with JC-1 flow cytometry; Figure 1C–H n = 4 and 1I n = 3; mean ± SD. No bar heights digitized. — Results 2.1; Figure 1C–I and caption; ROS Detection

Lipid peroxidation and cellular/mitochondrial ferrous iron: BDP probe and MDA assay, n = 3; Ferro-Orange, Fe2+ assay and Mito-FerroGreen, n = 5; mean ± SD. BDP panel B reports a Probe/Lipid fluorescence ratio, so its direction is interpreted with the probe images rather than relabeled as a direct lipid amount. — Results 2.2; Figure 2A–H and caption; Lipid Peroxidation Detection and Ferrous Ion Detection

NCOA4/LAMP1 colocalization and autolysosome counts: Immunofluorescence, Figure 2I n = 4; transmission electron microscopy/counting, Figure 2J n = 3; mean ± SD for counts. — Results 2.2; Figure 2I–J and caption; Immunofluorescence Staining and Transmission Electron Microscopy

In Vivo Studies

In male C57BL/6 mice, intravenous pinoresinol diglucoside at 5 or 10 mg/kg given 1 h before MCAO reduced neurological deficit, infarct volume and brain water content relative to saline-treated MCAO controls. Neurological scoring was performed 24 h after MCAO. The experiment evaluates pretreatment and does not establish benefit from post-stroke dosing. [2]

Intravenous PDG pretreatment in mouse cerebral ischemia/reperfusion

Animal study · Male C57BL/6 mice, 7–8 weeks, 20–23 g; sham, MCAO and MCAO + PDG groups; n = 9 assigned per group [2]

In one randomized four-group pretreatment experiment, PDG reduced neurological deficit, infarct volume and brain water content relative to saline-treated MCAO mice. This design tests prevention before ischemia, with short-term assessment, rather than treatment initiated after stroke.

Measured endpoints — not treatment concentrations
Endpoint	Reported result	Reference
Neurological deficit, brain infarct volume and brain water content	direction versus saline-treated MCAO Both 5 and 10 mg/kg PDG groups had lower mNSS scores, infarct volume and brain water content than the MCAO group (Figure 2 reports significance versus MCAO). No exact bar values inferred.	[2]

Conditions shared by the study groups

Route: Intravenous, caudal vein
Frequency: One administration described
Treatment course: 1 h before MCAO; neurological evaluation 24 h after MCAO
Vehicle: Normal saline

Study groups and reported outcomes
Group / dose	Comparator	Observed result	Reference
5 mg/kg PDG before MCAO 5 mg/kg	MCAO group received an equivalent volume of normal saline; sham group underwent the procedure without arterial occlusion.	Lower neurological deficit score, brain infarct volume and brain water content than the MCAO group. Exact effect sizes were not extracted from the graph.	[2]
10 mg/kg PDG before MCAO 10 mg/kg	MCAO group received an equivalent volume of normal saline; sham group underwent the procedure without arterial occlusion.	Lower neurological deficit score, brain infarct volume and brain water content than the MCAO group. Exact effect sizes were not extracted from the graph.	[2]

5 mg/kg PDG before MCAO: Model: Male C57BL/6 mouse MCAO/reperfusion model; Reported limits: No PDG-only sham arm; blinding, attrition and separate analyzed n per endpoint are not stated in the selected text.

10 mg/kg PDG before MCAO: Model: Male C57BL/6 mouse MCAO/reperfusion model; Reported limits: No PDG-only sham arm; blinding, attrition and separate analyzed n per endpoint are not stated in the selected text.

Methods and source locations

Compound reported in the paper: Pinoresinol diglucoside; Compound label in the paper: PDG; Jieshikang; purity ≥99%

Applies to the depicted and named diglucoside in this pretreatment mouse model; not to other pinoresinol glycoside isomers or clinical stroke treatment.

Methods 2.1–2.5 and 2.12; Results 3.1; Figures 1 and 2a–c

Neurological deficit, brain infarct volume and brain water content: mNSS 0–18 scale, with higher scores indicating greater deficit, assessed 24 h after MCAO; TTC-based infarct evaluation and dry/wet brain water measurement. Assigned group n = 9; endpoint-specific n is not separately stated in the figure caption. Statistics are described as mean ± SD. — Methods 2.1–2.5 and 2.12; Results 3.1; Figures 1 and 2a–c

5 mg/kg PDG before MCAO · Methods 2.1–2.5 and 2.12; Results 3.1; Figures 1 and 2a–c

10 mg/kg PDG before MCAO · Methods 2.1–2.5 and 2.12; Results 3.1; Figures 1 and 2a–c

Specifications

Manufacturer	Adooq Bioscience
CAS Number	63902-38-5
Formula	C₃₂H₄₂O₁₆
Molecular Weight	682.67
SMILES	COC1=C(C=CC(=C1)C2C3COC(C3CO2)C4=CC(=C(C=C4)OC5C(C(C(C(O5)CO)O)O)O)OC)OC6C(C(C(C(O6)CO)O)O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

Solvent	Reported Solubility
DMSO	93 mg/mL (136.23 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

[1] Yin Chen, Cheng Cheng, Ao Li, et al. Pinoresinol Diglucoside Attenuates Nuclear Receptor Coactivator 4‐Mediated Ferritinophagy Associated with Cisplatin‐Induced Hearing Loss Advanced Science (2025). PMID: 40051392 DOI: 10.1002/advs.202408777 Source material
[2] Yi Zhang, Yuanbiao Lei, Xiaoxi Yao, et al. Pinoresinol diglucoside alleviates ischemia/reperfusion‐induced brain injury by modulating neuroinflammation and oxidative stress Chemical Biology & Drug Design (2021). PMID: 34546621 DOI: 10.1111/cbdd.13956 Source material

Publications

1 publication citing this product

Mebeaselassie Andargie, .et al. , Molecules, 2021, Feb 7;26(4):883 PMID: 33562414

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Pinoresinol diglucoside

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