Guavinoside B
Guavinoside B is an orally active α-glucosidase inhibitor with an IC50 of 0.21 mM. Guavinoside B upregulates the expressions of Nrf2, GCLC and NQO1 induced by Acetaminophen (HY-66005), downregulates the expression of p-JNK, and reduces intracellular ROS levels. Guavinoside B decreases serum TNF-α levels induced by Acetaminophen, alleviates hepatocellular infiltration and necrosis, and improves liver-related biochemical parameters. Guavinoside B is applicable to the research of diabetes and Acetaminophen-induced liver injury.
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- CAS No.: 372955-18-5
- Formule: C28H28O13
- Masse moléculaire:572.51
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
IC50 & Target
[1]|
α‑glucosidase 0.21 mM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| A549 | IC50 |
10 μg/mL
Compound: Compound 9
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Cytotoxicity against human A549 cells by MTT assay
Cytotoxicity against human A549 cells by MTT assay
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[PMID: 25862199] |
In Vitro
Guavinoside B potently inhibits purified α-glucosidase enzyme activity with an IC50 of 0.21 mM[1].
Guavinoside B (3.3-100 μM; 24 h) does not affect the viability of HepG2 cells, either with or without 5 mM Acetaminophen (HY-66005) treatment[2].
Guavinoside B (3.3-30 μM; 16 h) reduces Acetaminophen-induced intracellular ROS accumulation by 28.6% in HepG2 cells, with weaker, non-significant effects at 3.3 and 10 μM[2].
Guavinoside B (10-30 μM; 16 h) upregulates Nrf2 and GCLC mRNA expression in untreated HepG2 cells, and (3.3-30 μM; 16 h) upregulates Nrf2, GCLC, and NQO1 mRNA expression in Acetaminophen-treated HepG2 cells[2].
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:HepG2 (human hepatocellular carcinoma cells)
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Concentration:3.3, 10, 30 μM (alone; co-treated with 5 mM Acetaminophen)
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Incubation Time:16 h
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Result:Increased mRNA expression levels of Nrf2 and GCLC at 10 and 30 μM when used alone.
Showed no impact on NQO1 mRNA expression when used alone.
Increased mRNA expression levels of Nrf2, GCLC, and NQO1 at 3.3, 10, and 30 μM when used with Acetaminophen.
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Cell Line:HepG2 (human hepatocellular carcinoma cells)
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Concentration:3.3, 10, 30 μM (alone; co-treated with 5 mM Acetaminophen)
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Incubation Time:16 h
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Result:Increased protein expression levels of Nrf2, GCLC, and NQO1 at 3.3, 10, and 30 μM when used alone.
Increased protein expression levels of Nrf2, GCLC, and NQO1 at 3.3, 10, and 30 μM when used with Acetaminophen compared to the Acetaminophen-only group.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 7 weeks old) injected with Acetaminophen[2]
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Dosage:100 mg/kg/d
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Administration:p.o.; daily; 7 consecutive days
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Result:Markedly alleviated Acetaminophen-induced hepatic pathological changes, including reduced hepatocyte necrosis and inflammation around central venous lesions.
Significantly reduced serum AST and ALT levels.
Significantly reduced hepatic ROS and MDA levels, and reversed Acetaminophen-induced depletion of hepatic GSH and SOD.
Significantly increased hepatic mRNA expression of SOD1 and GPx1.
Significantly up-regulated hepatic mRNA and protein expression levels of Nrf2, GCLC, and NQO1.
Significantly reduced serum TNF-α levels from 35.3 pg/mL (Acetaminophen-only group) to 27.3 pg/mL, and significantly inhibited Acetaminophen-induced JNK phosphorylation in liver tissue.
Chemical Information
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CAS No. 372955-18-5
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Masse moléculaire 572.51
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Formule C28H28O13
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SMILES
O=C(C1=CC=CC=C1)C2=C(C(C)=C(C(C)=C2O)O[C@@H]3O[C@@H]([C@H]([C@@H]([C@H]3O)O)O)COC(C4=CC(O)=C(C(O)=C4)O)=O)O
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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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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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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Pureté et documentation
Références
[1]. Xu L, et al. Inhibitory activity and mechanism of guavinoside B from guava fruits against α-glucosidase: Insights by spectroscopy and molecular docking analyses. J Food Biochem. 2022;46(7):e14101. [Content Brief]
[2]. Li Y, et al. Guavinoside B from Psidium guajava alleviates acetaminophen-induced liver injury via regulating the Nrf2 and JNK signaling pathways. Food Funct. 2020 Sep 23;11(9):8297-8308. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Guavinoside B Related Classifications
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