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MedChemExpress erastin

Nicotinamide <t>mononucleotide</t> <t>(NMN)</t> alleviated streptozotocin (STZ)-induced changes in INS-1 cell viability according to the CCK-8 assay. A , INS-1 cells were treated with various concentrations of STZ for 6 or 24 h. B , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 0, 50, 100, or 200 µM NMN for 24 h. C , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 10, 20, or 30 µM Fer-1 for 24 h. D , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with <t>erastin</t> (80, 100, or 120 µM) or 100 µM NMN for 24 h. Data are reported as means±SD (n=6). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Erastin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1092 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/erastin/Erastin/pmc13480942-50-25-26
Average 99 stars, based on 1092 article reviews

erastin - by Bioz Stars, 2026-09

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1) Product Images from "Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway"

Article Title: Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway

Journal: Brazilian Journal of Medical and Biological Research

doi: 10.1590/1414-431X2026e15295

Nicotinamide mononucleotide (NMN) alleviated streptozotocin (STZ)-induced changes in INS-1 cell viability according to the CCK-8 assay. A , INS-1 cells were treated with various concentrations of STZ for 6 or 24 h. B , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 0, 50, 100, or 200 µM NMN for 24 h. C , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 10, 20, or 30 µM Fer-1 for 24 h. D , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with erastin (80, 100, or 120 µM) or 100 µM NMN for 24 h. Data are reported as means±SD (n=6). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Figure Legend Snippet: Nicotinamide mononucleotide (NMN) alleviated streptozotocin (STZ)-induced changes in INS-1 cell viability according to the CCK-8 assay. A , INS-1 cells were treated with various concentrations of STZ for 6 or 24 h. B , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 0, 50, 100, or 200 µM NMN for 24 h. C , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 10, 20, or 30 µM Fer-1 for 24 h. D , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with erastin (80, 100, or 120 µM) or 100 µM NMN for 24 h. Data are reported as means±SD (n=6). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Techniques Used: CCK-8 Assay, Control

Nicotinamide mononucleotide (NMN) regulated streptozotocin (STZ)-induced ferroptosis in INS-1 cells by activating the Nrf2/GPX4 pathway. A , The mRNA expression levels of Keap1, Nrf2, and GPX4 were assessed by RT-qPCR, following treatment with STZ or NMN. B , The protein expression levels of Keap1, Nrf2, and GPX4 were assessed by western blot, following treatment with STZ or NMN. C , The mRNA expression levels of Nrf2 and GPX4 assessed by RT-qPCR, following treatment with STZ, Fer-1, erastin, or NMN. D , The protein expression levels of Nrf2 and GPX4 were assessed by western blot, following treatment with STZ, Fer-1, erastin, or NMN. Data are reported as means±SD (n=3). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Figure Legend Snippet: Nicotinamide mononucleotide (NMN) regulated streptozotocin (STZ)-induced ferroptosis in INS-1 cells by activating the Nrf2/GPX4 pathway. A , The mRNA expression levels of Keap1, Nrf2, and GPX4 were assessed by RT-qPCR, following treatment with STZ or NMN. B , The protein expression levels of Keap1, Nrf2, and GPX4 were assessed by western blot, following treatment with STZ or NMN. C , The mRNA expression levels of Nrf2 and GPX4 assessed by RT-qPCR, following treatment with STZ, Fer-1, erastin, or NMN. D , The protein expression levels of Nrf2 and GPX4 were assessed by western blot, following treatment with STZ, Fer-1, erastin, or NMN. Data are reported as means±SD (n=3). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Control

CCK-8 Assay:

Article Title: Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway
Article Snippet: .. The cells were treated with different concentrations of STZ (Solarbio) for 6 or 24 h. Then, the cells were washed with PBS and treated with erastin (MedChemExpress, China), ferrostatin-1 (Fer-1, MedChemExpress), or NMN (Sigma-Aldrich, USA) for 24 h. The cells were subsequently treated with 10 μL of CCK-8 reagent and incubated for 1 h at 37°C. .. The absorbance was measured at 450 nm using a microplate reader (Fluoroskan AscentTM; Thermo Fisher Scientific, Inc.), after which the cell viability was calculated based on the absorbance.

Incubation:

Transfection:

Article Title: NOV promotes renal ischemia-reperfusion injury by driving TFRC-dependent ferroptosis.
Article Snippet: Acute kidney injury (AKI) is a severe clinical syndrome with limited therapeutic options, and its underlying molecular mechanisms remain incompletely understood.. Nephroblastoma overexpressed (NOV), a matricellular protein, has been implicated in renal pathophysiology; however, its role in AKI remains unclear.. Using a murine renal ischemia-reperfusion (I/R) model and HK-2 cells subjected to hypoxia/reoxygenation (H/R), we found that NOV was rapidly induced in renal tubular epithelial cells (RTECs) during the early phase of AKI.

Control:

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Journal: Brazilian Journal of Medical and Biological Research

Article Title: Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway

doi: 10.1590/1414-431X2026e15295

Figure Lengend Snippet: Nicotinamide mononucleotide (NMN) alleviated streptozotocin (STZ)-induced changes in INS-1 cell viability according to the CCK-8 assay. A , INS-1 cells were treated with various concentrations of STZ for 6 or 24 h. B , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 0, 50, 100, or 200 µM NMN for 24 h. C , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with 10, 20, or 30 µM Fer-1 for 24 h. D , INS-1 cells were treated with 0.25 mM STZ for 6 h, and then treated with erastin (80, 100, or 120 µM) or 100 µM NMN for 24 h. Data are reported as means±SD (n=6). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Article Snippet: The cells were treated with different concentrations of STZ (Solarbio) for 6 or 24 h. Then, the cells were washed with PBS and treated with erastin (MedChemExpress, China), ferrostatin-1 (Fer-1, MedChemExpress), or NMN (Sigma-Aldrich, USA) for 24 h. The cells were subsequently treated with 10 μL of CCK-8 reagent and incubated for 1 h at 37°C.

Techniques: CCK-8 Assay, Control

Journal: Brazilian Journal of Medical and Biological Research

Article Title: Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway

doi: 10.1590/1414-431X2026e15295

Figure Lengend Snippet: Nicotinamide mononucleotide (NMN) regulated streptozotocin (STZ)-induced ferroptosis in INS-1 cells by activating the Nrf2/GPX4 pathway. A , The mRNA expression levels of Keap1, Nrf2, and GPX4 were assessed by RT-qPCR, following treatment with STZ or NMN. B , The protein expression levels of Keap1, Nrf2, and GPX4 were assessed by western blot, following treatment with STZ or NMN. C , The mRNA expression levels of Nrf2 and GPX4 assessed by RT-qPCR, following treatment with STZ, Fer-1, erastin, or NMN. D , The protein expression levels of Nrf2 and GPX4 were assessed by western blot, following treatment with STZ, Fer-1, erastin, or NMN. Data are reported as means±SD (n=3). *P<0.05 compared with the control group; # P<0.05 compared with the 0.25 mM STZ group (ANOVA).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control

Curcumin rescues Erastin induced ferroptosis and restores decidualization in telomerase‐immortalized human endometrial stromal cells (T hESCs). (A) Representative transmission electron microscopy (TEM) images of mitochondrial ultrastructure in T hESCs under indicated treatments indicated shrunken mitochondria with condensed membranes, characteristic of ferroptosis. (B–D) Biochemical assessment of ferroptosis markers: Malondialdehyde (MDA) content (B), superoxide dismutase (SOD) activity (C), and the reduced/oxidized glutathione (GSH/GSSG) ratio (D) ( n = 6). (E–H) Representative immunofluorescence images showing intracellular ferrous iron (Fe 2+ ) (E), and expression of TFRC (F), ACSL4 (G), and SLC7A11 (H) (scale bar: 50 μm). (I–L) Quantification of fluorescence intensity for Fe 2+ (I), TFRC (J), ACSL4 (K), and SLC7A11 (L) ( n = 3). (M, N) ELISA was used to quantify the level of IGFBP1 (M) and PRL (N) from each group ( n = 6). Data are presented as means ± SEM. Statistical significance is determined by one‐way ANOVA (Dunnett's post‐test). ** p < 0.01 (normal control vs. model group); # p < 0.05, ## p < 0.01 (treatment groups vs. model group).

Journal: Food Science & Nutrition

Article Title: Curcumin Attenuates Decidual Stromal Cell Ferroptosis and Restores Impaired Decidualization in Recurrent Spontaneous Abortion by Targeting BRD4

doi: 10.1002/fsn3.72205

Figure Lengend Snippet: Curcumin rescues Erastin induced ferroptosis and restores decidualization in telomerase‐immortalized human endometrial stromal cells (T hESCs). (A) Representative transmission electron microscopy (TEM) images of mitochondrial ultrastructure in T hESCs under indicated treatments indicated shrunken mitochondria with condensed membranes, characteristic of ferroptosis. (B–D) Biochemical assessment of ferroptosis markers: Malondialdehyde (MDA) content (B), superoxide dismutase (SOD) activity (C), and the reduced/oxidized glutathione (GSH/GSSG) ratio (D) ( n = 6). (E–H) Representative immunofluorescence images showing intracellular ferrous iron (Fe 2+ ) (E), and expression of TFRC (F), ACSL4 (G), and SLC7A11 (H) (scale bar: 50 μm). (I–L) Quantification of fluorescence intensity for Fe 2+ (I), TFRC (J), ACSL4 (K), and SLC7A11 (L) ( n = 3). (M, N) ELISA was used to quantify the level of IGFBP1 (M) and PRL (N) from each group ( n = 6). Data are presented as means ± SEM. Statistical significance is determined by one‐way ANOVA (Dunnett's post‐test). ** p < 0.01 (normal control vs. model group); # p < 0.05, ## p < 0.01 (treatment groups vs. model group).

Article Snippet: Curcumin (MedChemExpress, Cat. No.: HY‐N0005), Dydrogesterone (MedChemExpress, Cat. No.: HY‐B0257A), Erastin (MedChemExpress, Cat. No.: HY‐15763), JQ‐1 (MedChemExpress, Cat. No.: HY‐13030), 8‐bromoadenosine 3′, 5′‐cyclic monophosphate (8‐Br‐cAMP) (Sigma, Cat. No.: B5386), Medroxyprogesterone acetate (MPA) (APExBIO, Cat. No.: B1510), DMEM/F12 (Thermo Fisher, Cat. No.: 12634010), Fetal bovine serum (FBS) (Gibco, Cat. No.: 10099141); rLV‐CMV‐BRD4‐PGK‐Puro‐WPRE (BrainVTA Co. Ltd., Wuhan, China); CoraLite594‐Phalloidin (red) (Proteintech, Cat. No.: PF00003), FeRhoNox‐1 (Fe 2+ indicator) (Maokangbio, Cat. No.: MX4558); mouse MDA ELISA kit (BYabscience, Cat. No.: BY‐WJZF0071), mouse SOD ELISA kit (BYabscience, Cat. No.: BY‐ EM221637 ), mouse PRL ELISA kit (BYabscience, Cat. No.: BY‐ EM220246 ), mouse IGFBP1 ELISA kit (BYabscience, Cat. No.: BY‐ EM228061 ), human MDA ELISA kit (BYabscience, Cat. No.: BY‐WJZF0118), human SOD ELISA kit (BYabscience, Cat. No.: BY‐ EH112140 ), human PRL ELISA kit (BYabscience, Cat. No.: BY‐ EH110473 ), human IGFBP1 ELISA kit (BYabscience, Cat. No.: BY‐ EH114674 ), GSH ELISA kit (BYabscience, Cat. No.: BY‐WJZF0366), GSSG ELISA kit (BYabscience, Cat. No.: BY‐WJZF1210).

Techniques: Transmission Assay, Electron Microscopy, Activity Assay, Immunofluorescence, Expressing, Fluorescence, Enzyme-linked Immunosorbent Assay, Control

Inhibition of TP53 mitigates SCI-induced ferroptosis. (A) Tissue iron content in the spinal cords of the three groups at 14 dpi ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (B) Prussian blue staining (enhanced with 3,3′-diaminobenzidine) of spinal cord sections from the three groups at 14 dpi. (C) MDA detection in injured spinal cords at 14 dpi ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (D) Immunofluorescence images of 4HNE (red) and NeuN (green) cells at 14 dpi. (E, F) Quantification of 4HNE immunofluorescence ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (G) Colocalization analysis of 4HNE and NeuN in the dashed box of the SCI group. (H) Transmission electron microscopy images of mitochondria in the spinal cords of the three groups at 14 dpi. (I) Ptgs2 mRNA levels in the three groups were detected via qPCR at 14 dpi ( n = 5, one-way ANOVA followed by Tukey’s multiple comparison test). (J, K) Western blot bands (J) and quantification (K) of PTGS2 expression in the three groups at 14 dpi ( n = 5, one-way ANOVA followed by Tukey’s multiple comparison test). The values are presented as the mean ± SD. *** P < 0.001. 4HNE: 4-Hydroxynonenal; ANOVA: analysis of variance; DAPI: 4′,6-diamidino-2-phenylindole; dpi: days post-injury; FA: fluorescence area; MDA: malondialdehyde; MFI: mean fluorescence intensity; NeuN: neuronal nuclei; ns: not significant; Pft-α: pifithrin-α (TP53 inhibitor); PTGS2: prostaglandin-endoperoxide synthase 2; SCI: spinal cord injury.

Journal: Neural Regeneration Research

Article Title: TP53 drives neuronal ferroptosis by promoting KLHL4-mediated SLC7A11 ubiquitination after spinal cord injury

doi: 10.4103/NRR.NRR-D-24-01612

Figure Lengend Snippet: Inhibition of TP53 mitigates SCI-induced ferroptosis. (A) Tissue iron content in the spinal cords of the three groups at 14 dpi ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (B) Prussian blue staining (enhanced with 3,3′-diaminobenzidine) of spinal cord sections from the three groups at 14 dpi. (C) MDA detection in injured spinal cords at 14 dpi ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (D) Immunofluorescence images of 4HNE (red) and NeuN (green) cells at 14 dpi. (E, F) Quantification of 4HNE immunofluorescence ( n = 5; one-way ANOVA followed by Tukey’s multiple comparison test). (G) Colocalization analysis of 4HNE and NeuN in the dashed box of the SCI group. (H) Transmission electron microscopy images of mitochondria in the spinal cords of the three groups at 14 dpi. (I) Ptgs2 mRNA levels in the three groups were detected via qPCR at 14 dpi ( n = 5, one-way ANOVA followed by Tukey’s multiple comparison test). (J, K) Western blot bands (J) and quantification (K) of PTGS2 expression in the three groups at 14 dpi ( n = 5, one-way ANOVA followed by Tukey’s multiple comparison test). The values are presented as the mean ± SD. *** P < 0.001. 4HNE: 4-Hydroxynonenal; ANOVA: analysis of variance; DAPI: 4′,6-diamidino-2-phenylindole; dpi: days post-injury; FA: fluorescence area; MDA: malondialdehyde; MFI: mean fluorescence intensity; NeuN: neuronal nuclei; ns: not significant; Pft-α: pifithrin-α (TP53 inhibitor); PTGS2: prostaglandin-endoperoxide synthase 2; SCI: spinal cord injury.

Article Snippet: The feasibility of the cell model was validated using a ferroptosis inducer (erastin, HY-15763, MCE, Shanghai, China) and inhibitor (ferrostatin-1, HY-100579, MCE).

Techniques: Inhibition, Comparison, Staining, Immunofluorescence, Transmission Assay, Electron Microscopy, Western Blot, Expressing, Fluorescence

TP53 manipulates ferroptosis induced by H 2 O 2 and Fe in PC12 cells. (A–E) Western blot bands (A) and quantification (B–E) of SLC7A11, TP53, GPX4 and 4HNE ( n = 3, ANOVA followed by Tukey’s multiple comparison test). (F) Immunofluorescence images and quantitative statistics (G) of TP53 in PC12 cells ( n = 3; one-way ANOVA followed by Tukey’s multiple comparison test). (H) Immunofluorescence images and quantitative statistics (I) of SLC7A11 in PC12 cells ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (J) Flow cytometry detection and quantification (K) of ROS ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (L) Fluorescence images and quantification (M) of C11-BODIPY (581/591) ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (N) Intracellular ferric ion content determination ( n = 3; one-way ANOVA followed by Tukey’s multiple comparison test). (O) Fluorescence images and quantitation (P) of FerroOrange ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (Q) Transmission electron microscopy images of mitochondria in PC12 cells. The boxed border regions are enlarged. The values are plotted as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. 4HNE: 4-Hydroxynonenal; ANOVA: analysis of variance; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; GPX4: glutathione peroxidase 4; MFI: mean fluorescence intensity; ns: not significant; O/E: overexpression; ROS: reactive oxygen species; TP53: tumor protein 53.

Journal: Neural Regeneration Research

Article Title: TP53 drives neuronal ferroptosis by promoting KLHL4-mediated SLC7A11 ubiquitination after spinal cord injury

doi: 10.4103/NRR.NRR-D-24-01612

Figure Lengend Snippet: TP53 manipulates ferroptosis induced by H 2 O 2 and Fe in PC12 cells. (A–E) Western blot bands (A) and quantification (B–E) of SLC7A11, TP53, GPX4 and 4HNE ( n = 3, ANOVA followed by Tukey’s multiple comparison test). (F) Immunofluorescence images and quantitative statistics (G) of TP53 in PC12 cells ( n = 3; one-way ANOVA followed by Tukey’s multiple comparison test). (H) Immunofluorescence images and quantitative statistics (I) of SLC7A11 in PC12 cells ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (J) Flow cytometry detection and quantification (K) of ROS ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (L) Fluorescence images and quantification (M) of C11-BODIPY (581/591) ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (N) Intracellular ferric ion content determination ( n = 3; one-way ANOVA followed by Tukey’s multiple comparison test). (O) Fluorescence images and quantitation (P) of FerroOrange ( n = 3, one-way ANOVA followed by Tukey’s multiple comparison test). (Q) Transmission electron microscopy images of mitochondria in PC12 cells. The boxed border regions are enlarged. The values are plotted as the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001. 4HNE: 4-Hydroxynonenal; ANOVA: analysis of variance; DAPI: 4′,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; GPX4: glutathione peroxidase 4; MFI: mean fluorescence intensity; ns: not significant; O/E: overexpression; ROS: reactive oxygen species; TP53: tumor protein 53.

Article Snippet: The feasibility of the cell model was validated using a ferroptosis inducer (erastin, HY-15763, MCE, Shanghai, China) and inhibitor (ferrostatin-1, HY-100579, MCE).

Techniques: Western Blot, Comparison, Immunofluorescence, Flow Cytometry, Fluorescence, Quantitation Assay, Transmission Assay, Electron Microscopy, Over Expression

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erastin (MedChemExpress)

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1) Product Images from "Nicotinamide mononucleotide alleviates the streptozotocin-mediated ferroptosis of islet β-cells via the Nrf2/GPX4 pathway"

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