2. Membrane Transporter/Ion Channel Apoptosis Autophagy Immunology/Inflammation NF-κB Metabolic Enzyme/Protease
  3. Potassium Channel Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism
  4. Cereulide

Cereulide is an orally active, blood-brain barrier-permeable emetic toxin. Cereulide acts as a potassium ionophore that inserts into membranes, forms complexes with K+, and transports K+ from the cytoplasm into the mitochondrial matrix. Cereulide disrupts the electrochemical gradient of the inner mitochondrial membrane, leading to mitochondrial swelling and dysfunction, uncoupling of oxidative phosphorylation, inhibition of ATP synthesis, ROS accumulation, and ultimately triggering apoptosis and autophagy. Cereulide exhibits multi-organ toxicity and can be used for research on emetic food poisoning.

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Cereulide

Cereulide Chemical Structure

CAS No. : 157232-64-9

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Other Forms of Cereulide:

Cereulide Related Antibodies

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Description

Cereulide is an orally active, blood-brain barrier-permeable emetic toxin. Cereulide acts as a potassium ionophore that inserts into membranes, forms complexes with K+, and transports K+ from the cytoplasm into the mitochondrial matrix. Cereulide disrupts the electrochemical gradient of the inner mitochondrial membrane, leading to mitochondrial swelling and dysfunction, uncoupling of oxidative phosphorylation, inhibition of ATP synthesis, ROS accumulation, and ultimately triggering apoptosis and autophagy. Cereulide exhibits multi-organ toxicity and can be used for research on emetic food poisoning[1][2][3][4].

In Vitro

Cereulide (<1 ng/mL, chronic; 0.05-0.5 nM, 10 days; 0.2-500 nM, 24 h) induces mitochondrial dysfunction, impairs intestinal barrier function, inhibits cell proliferation, and triggers inflammation in Caco-2 cells, with maximal respiration reduced to 2% of baseline and ATP production to 6% of baseline at 0.5 nM after 10 days of exposure[1].
Cereulide (0.05-0.5 ng/mL, 24 h; 1 ng/mL, 2 days; 10 ng/mL, 8-24 h) dose-dependently impairs glucose-stimulated insulin secretion and induces apoptosis and necrosis in MIN6 cells and pancreatic islets, with complete loss of insulin secretion at 0.25 ng/mL in MIN6 cells after 24 h of exposure[1].
Cereulide (0.05-0.5 nM, 10 days) induces severe mitochondrial dysfunction in HepG2 cells, with maximal respiration reduced to 2% of baseline and ATP production to 6% of baseline at 0.5 nM after 10 days of exposure[1].
Cereulide (20 ng/mL, 1 min; 100-1000 ng/mL, 3 h; unspecified, 1 day) rapidly impairs cytotoxic function, induces mitochondrial damage, and triggers apoptosis in NK cells, with loss of cytotoxic capacity observed within 1 min of exposure to 20 ng/mL[1].
Cereulide (2.74-2.98 ng/mL; 24 h) reduces viability of HepaRG cells with an IC50 of 2.98 ng/mL and HEK293T cells with an IC50 of 2.74 ng/mL after 24 h of treatment[2].
Cereulide (0.3-1 ng/mL; 24 h) induces dose-dependent apoptosis in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 24 h) induces structural damage including mitochondrial dysfunction and apoptotic morphological changes in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 24 h) induces ER swelling in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 3-24 h) activates the IRE1α/XBP1 and PERK/eIF2α ER stress pathways and upregulates pro-apoptotic CHOP in a time- and dose-dependent manner in HepaRG and HEK293T cells after treatment with 0.3 or 1 ng/mL for 3, 6, or 24 h[2].
Cereulide (0.3-1 ng/mL; 24 h) induces dose-dependent ROS accumulation in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.5-1 ng/mL; 4 h) induces ER stress (increased p-eIF2α and CHOP) in HepaRG and HEK293T cells treated with 1 ng/mL or 0.5 ng/mL for 4 h that is mediated by ROS accumulation[2].
Cereulide (1 ng/mL; 48 h) reduces insulin content and increases cell death in fetal porcine islets of Langerhans[3].
Cereulide (10 ng/mL; 8-24 h) induces loss of mitochondrial membrane potential and necrotic/pyknotic cell death in murine insulinoma MIN6 cells[3].
Cereulide (5 ng/mL; 24 h) induces high rates of apoptosis in rat INS-1E cells, murine insulinoma MIN6 cells, and freshly isolated murine pancreatic islets[3].
Cereulide (0.5 ng/mL; 24 h) impairs mitochondrial structure and function, increases reactive oxygen species, and induces apoptosis in murine insulinoma MIN6 cells[3].
Cereulide (0.15-0.5 ng/mL; 24 h) significantly reduces or completely inhibits glucose-stimulated insulin secretion in murine insulinoma MIN6 cells and freshly isolated murine pancreatic islets[3].
Cereulide (2 nM) inhibits RNA synthesis in human hepatocellular carcinoma HepG2 cells[3].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) reduces cell viability of HepG2 liver cells in a concentration- and time-dependent manner, with cytotoxicity observed at lower concentrations after 24 h compared to 5 h[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) alters mitochondrial quantity and morphology in HepG2 liver cells, with an initial increase in mitochondrial number at 0.1 ng/mL followed by concentration-dependent decreases at higher concentrations, and mitochondrial aberrations detected at 2.5 ng/mL after 24 h[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) increases lysosomal number and/or size in HepG2 liver cells at concentrations 0.1-5 ng/mL after 5 and 24 h, with a maximum increase to 136% of solvent control at 2.5 ng/mL after 24 h, while higher concentrations reduce lysosomal signal[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) increases lysosomal acidification in HepG2 liver cells at concentrations 2.5-50 ng/mL after 24 h, with no significant effects detected after 5 h[4].
Cereulide (0.1-1 ng/mL; 5 h, 24 h) upregulates transcription of autophagy-related genes MAP1LC3B and SQSTM1 in HepG2 liver cells at 1 ng/mL after 5 and 24 h, while marginally reducing transcription of lysosomal and other autophagy-related genes[4].
Cereulide (0.1-1 ng/mL; 24 h) increases LC3 protein expression in HepG2 liver cells at 0.1 and 1 ng/mL after 24 h, indicating induction of autophagy via the LC3 pathway[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cereulide Related Antibodies

Apoptosis Analysis[2]

Cell Line: HepaRG cells, HEK293T cells
Concentration: 0.3 and 1 ng/mL
Incubation Time: 24 h
Result: Caused a dose-dependent significant increase in the number of apoptotic cells in both HepaRG and HEK293T cells.

Western Blot Analysis[2]

Cell Line: HepaRG cells, HEK293T cells
Concentration: 0.3 and 1 ng/mL
Incubation Time: 3, 6 and 24 h
Result: Caused time- and dose-dependent increases in phosphorylation of IRE1α and PERK, phosphorylation of eIF2α, levels of XBP1(s), and levels of CHOP in both cell lines.
Did not increase BiP levels at 3 h or 6 h, but significantly increased BiP levels at 24 h.

Western Blot Analysis[2]

Cell Line: HepaRG cells, HEK293T cells
Concentration: 0.5 ng/mL (HEK293T cells); 1 ng/mL (HepaRG cells)
Incubation Time: 4 h
Result: Induced increases in p-eIF2α and CHOP levels that were reversed by NAC pretreatment in both cell lines.

Apoptosis Analysis[3]

Cell Line: Murine insulinoma MIN6 cells
Concentration: 0.5 ng/mL
Incubation Time: 24 h
Result: Caused swollen, disintegrated mitochondria in murine insulinoma MIN6 cells.
Increased reactive oxygen species by more than twofold in murine insulinoma MIN6 cells.
Reduced basal respiration rate to half in murine insulinoma MIN6 cells.
Increased caspase 3/7 activation in murine insulinoma MIN6 cells.
Elevated cytochrome C release into the cytoplasm in murine insulinoma MIN6 cells.
Upregulated pro-apoptotic mRNA markers including CHOP in murine insulinoma MIN6 cells.

Cell Viability Assay[4]

Cell Line: HepG2 liver cells
Concentration: 0.1, 1, 2.5, 5, 10 and 50 ng/mL
Incubation Time: 5 h; 24 h
Result: Reduced cell viability to approximately 65-70% starting from 2.5 ng/mL after 5 h incubation.
Reduced cell viability to 46% at the highest tested concentration after 24 h incubation.

Real Time qPCR[4]

Cell Line: HepG2 liver cells
Concentration: 0.1, 1, 2.5, 5, 10 and 50 ng/mL
Incubation Time: 5 h; 24 h
Result: Increased MAP1LC3B and SQSTM1 transcript levels at 1 ng/mL after 5 h incubation.
Marginally reduced LAMP2, CTSD, and ATG16 transcript levels at 0.1 and 1 ng/mL after 5 h incubation.
Increased MAP1LC3B transcript levels to ~2.7-fold of solvent control at 1 ng/mL after 24 h incubation.
Increased SQSTM1 transcript levels to ~2.5-fold of solvent control at 1 ng/mL after 24 h incubation.
Reduced CTSD transcript levels to below 0.5-fold of solvent control at 1 ng/mL after 24 h incubation.
Marginally reduced LAMP2 and ATG16 transcript levels at 0.1 and 1 ng/mL after 24 h incubation.

Immunofluorescence[4]

Cell Line: HepG2 liver cells
Concentration: 0.1 and 1 ng/mL
Incubation Time: 24 h
Result: Increased LC3 fluorescence intensity to ~130% of solvent control at 0.1 ng/mL after 24 h incubation.
Increased LC3 fluorescence intensity to ~150% of solvent control at 1 ng/mL after 24 h incubation, similar to the positive control rapamycin.
In Vivo

Cereulide (10-200 μg/kg; p.o.; once daily; 28 days) induces oxidative stress, inflammatory responses, endoplasmic reticulum stress and subsequent apoptosis via the IRE1α/XBP1 and PERK/eIF2α pathways, thereby causing hepatic and renal function injury in male BALB/c mice[2].
Cereulide (10-20 μg per mouse; i.p.; single administration) induces dose-dependent hepatotoxicity in male BALB/c mice, with 20 μg being a lethal dose, 10 μg causing reversible toxicity, and 15 μg leading to significant liver injury[3].
Cereulide-containing *Bacillus cereus* cultures induce microvesicular steatosis and midzonal necrosis in rat livers, replicating fatal human hepatotoxicity[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c (6-week-old, male, SPF, acclimated for 1 week post-purchase)[2]
Dosage: 10 μg/kg; 50 μg/kg; 200 μg/kg
Administration: p.o.; daily; 28 days
Result: Significantly decreased body weight; increased kidney and spleen indices; induced hepatocyte and glomerular swelling, inflammatory cell infiltration; increased mRNA levels of IL-6 and TNF-α in liver and kidney; significantly decreased SOD activity in liver and kidney; significantly increased MDA level in liver; increased mRNA levels of XBP1(s) and ATF4, and increased protein/phosphorylation levels of IRE1α/XBP1(s) and PERK/eIF2α/CHOP in liver and kidney; reached ~20% TUNEL-positive apoptotic cells in liver and ~22% in kidney (50 μg/kg).
Animal Model: BALB/c (male)[3]
Dosage: 20 μg; 15 μg; 10 μg
Administration: i.p.; single dose
Result: Caused lethality at 20 μg
Induced marked hepatocyte swelling (due to mitochondrial swelling) and elevation of serum transaminases at 15 μg.
Allowed full recovery 4 weeks after 10 μg.
Molecular Weight

1153.40

Formula

C57H96N6O18
CAS No.
Appearance

Solid

Color

White to off-white

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Room temperature in continental US; may vary elsewhere.
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Powder -80°C 2 years
-20°C 1 year

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (86.70 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 0.8670 mL 4.3350 mL 8.6700 mL
5 mM 0.1734 mL 0.8670 mL 1.7340 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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Purity & Documentation
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 0.8670 mL 4.3350 mL 8.6700 mL 21.6750 mL
5 mM 0.1734 mL 0.8670 mL 1.7340 mL 4.3350 mL
10 mM 0.0867 mL 0.4335 mL 0.8670 mL 2.1675 mL
15 mM 0.0578 mL 0.2890 mL 0.5780 mL 1.4450 mL
20 mM 0.0434 mL 0.2168 mL 0.4335 mL 1.0838 mL
25 mM 0.0347 mL 0.1734 mL 0.3468 mL 0.8670 mL
30 mM 0.0289 mL 0.1445 mL 0.2890 mL 0.7225 mL
40 mM 0.0217 mL 0.1084 mL 0.2168 mL 0.5419 mL
50 mM 0.0173 mL 0.0867 mL 0.1734 mL 0.4335 mL
60 mM 0.0145 mL 0.0723 mL 0.1445 mL 0.3613 mL
80 mM 0.0108 mL 0.0542 mL 0.1084 mL 0.2709 mL
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Cereulide Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Cereulide157232-64-9Potassium ChannelApoptosisAutophagyReactive Oxygen Species (ROS)Mitochondrial MetabolismKcsATPH-1NK cells5-HT3 receptorsIRE1α/XBP1Caco-2 cellsTPH-2HepG2 cellsMIN6 cellspancreatic beta cellsPERK/eIF2αInhibitorinhibitorinhibit

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