m ferrostatin 1  (MedChemExpress)

Journal: International Journal of Molecular Medicine

Article Title: HELLS inhibits autophagy-dependent ferroptosis in nasopharyngeal carcinoma by modulating the Nrf2/HO-1/GPX4 pathway

doi: 10.3892/ijmm.2026.5788

Figure Lengend Snippet: Effects of HELLS on ferroptosis. Levels of (A) GSH, (B) MDA and (C) Fe 2+ in the sh-HELLS, sh-NC, sh-HELLS + Era, sh-NC + Era, sh-HELLS + Era + Fer-1 and sh-NC + Era + Fer-1 groups. (D) Representative images illustrating immunofluorescence staining of ROS probes in the six groups. (E) ROS levels in the six groups. (F and G) Relative mRNA expression levels of (F) ACSL4 and (G) PTGS2 in the six groups. (H) Representative images of immunoblots of 4-HNE, ACSL4 and PTGS2. (I) Relative expression levels of 4-HNE in the six groups. (J and K) Relative protein expression levels of (J) ACSL4 and (K) PTGS2 in the six groups. * P<0.05, ** P<0.01, *** P<0.001 and **** P<0.0001. HELLS, lymphoid-specific helicase; GSH, glutathione; MDA, malondialdehyde; sh-, short hairpin; NC, negative control; Era, erastin; Fer-1, ferrostatin-1; ROS, reactive oxygen species; 4-HNE, 4-hydroxynonenal; ACSL4, acyl-CoA synthetase long-chain family member 4; PTGS2, prostaglandin-endoperoxide synthase 2.

Article Snippet: To modulate ferroptosis, cells transfected with sh-NC and sh-HELLS sequences were treated for 24 h with either 10 μ M of erastin (cat. no. HY-15763; MedChemExpress) or a combination of 10 μ M of Erastin and 2 μ M ferrostatin-1 (Fer-1; cat. no. HY-100579; MedChemExpress) ( , ).

Techniques: Immunofluorescence, Staining, Expressing, Western Blot, Negative Control

Journal: International Journal of Molecular Medicine

Article Title: Unveiling the role of RhoA and ferroptosis in vascular permeability: Implications for osteoarthritis

doi: 10.3892/ijmm.2024.5410

Figure Lengend Snippet: Animal experiment workflow. Mice were randomly divided into four groups (n=15/group) and sampled at 4 and 8 weeks for serum and histological examination. DMM, destabilization of the medial meniscus; CT, micro-computed tomography; Fer, Ferrostatin-1.

Article Snippet: ECs were stimulated with interleukin-1β (100 ng/ml) for 24 h with or without 50 μ M ferroptosis inhibitor ferrostatin-1 or 10 μ M ferroptosis activator erastin at 37°C (all MedChemExpress).

Techniques: Micro-CT

Journal: International Journal of Molecular Medicine

Article Title: Unveiling the role of RhoA and ferroptosis in vascular permeability: Implications for osteoarthritis

doi: 10.3892/ijmm.2024.5410

Figure Lengend Snippet: Ferroptosis inhibition reverses IL-1β-induced increase in EC permeability. ECs were incubated with IL-1β alone or combination with Fer-1 for 24 h. Representative immunofluorescence staining for (A) ZO-1 and (B) connexin 43. Scale bar, 50 μ m. Quantitative analysis of (C) ZO-1 and (D) connexin 43 fluorescence intensity. Reverse transcription-quantitative PCR to detect (E) ZO-1 and (F) connexin 43 mRNA expression. n=5. (G) Western blotting for (H) ZO-1 and (I) connexin 43 protein expression. (J) Immunofluorescence staining for EC cytoskeletal F-actin (dashed line). (K) Immunofluorescence staining for VE-cadherin (arrow). Scale bar, 20 μ m. (L) Migration of ECs in scratch assay. Scale bar, 500 μ m. (M) Quantitative analysis of cell migration in scratch assay. n=3. *** P<0.001. EC, endothelial cell; Fer-1, Ferrostatin-1; ZO-1, Zona occludens-1; VE-, vascular endothelial-cadherin.

Article Snippet: ECs were stimulated with interleukin-1β (100 ng/ml) for 24 h with or without 50 μ M ferroptosis inhibitor ferrostatin-1 or 10 μ M ferroptosis activator erastin at 37°C (all MedChemExpress).

Techniques: Inhibition, Permeability, Incubation, Immunofluorescence, Staining, Fluorescence, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Migration, Wound Healing Assay

Journal: International Journal of Molecular Medicine

Article Title: Unveiling the role of RhoA and ferroptosis in vascular permeability: Implications for osteoarthritis

doi: 10.3892/ijmm.2024.5410

Figure Lengend Snippet: RhoA or ferroptosis inhibition alleviates cartilage degeneration in mice with DMM. (A) H&E, (B) S-F and (C) Masson's staining of knee joints in DMM mice after RhoA or ferroptosis inhibition. Black line, HC thickness; white, CC. Scale bar, 100 and 50 μ m. Quantitative analysis of (D) HC and (E) CC thickness in H&E-stained samples and (F) OARSI scores of knee joint cartilage using S-F staining. n=5. * P<0.05, ** P<0.01 and *** P<0.001. RhoA, Ras homolog family member A; DMM, destabilization of the medial meniscus; H&E, hematoxylin and eosin; S-F, Safranin-O-fast green; HC, Hyaline cartilag; CC, Calcified cartilage; OARSI, Osteoarthritis Research Society International; Fer-1, Ferrostatin-1.

Article Snippet: ECs were stimulated with interleukin-1β (100 ng/ml) for 24 h with or without 50 μ M ferroptosis inhibitor ferrostatin-1 or 10 μ M ferroptosis activator erastin at 37°C (all MedChemExpress).

Techniques: Inhibition, Staining

Journal: International Journal of Molecular Medicine

Article Title: Unveiling the role of RhoA and ferroptosis in vascular permeability: Implications for osteoarthritis

doi: 10.3892/ijmm.2024.5410

Figure Lengend Snippet: RhoA or ferroptosis inhibition rescues subchondral bone remodeling in DMM mice. (A) Two-dimensional micro-CT scan of the tibial subchondral bone. Magnification: ×10. (B) Representative three-dimensional micro-CT reconstructed images of mouse knee joints. Magnification: ×10. (C) Two-dimensional micro-CT reconstruction of the tibial subchondral bone. Magnification: ×10. (D) BV/TV. (E) Tb.Sp. (F) TMD. (G) Tb.Th. n=5. ** P<0.01 and *** P<0.001. RhoA, Ras homolog family member A; DMM, destabilization of the medial meniscus; CT, micro-computed tomography; BV/TV, bone volume/total volume; Tb.Sp, trabecular separation; TMD, tissue mineral density; Tb.Th, trabecular thickness; Fer-1, Ferrostatin-1.

Article Snippet: ECs were stimulated with interleukin-1β (100 ng/ml) for 24 h with or without 50 μ M ferroptosis inhibitor ferrostatin-1 or 10 μ M ferroptosis activator erastin at 37°C (all MedChemExpress).

Techniques: Inhibition, Micro-CT

Journal: Journal of Oncology

Article Title: MCT4 Promotes Tumor Malignancy in F98 Glioma Cells

doi: 10.1155/2021/6655529

Figure Lengend Snippet: Cell cycle profiles and cell death mechanisms in MCT4 overexpression and knockdown F98 glioma cells. (a) Cell cycle analysis of con, MCT4, and MCT4 KD F98 cells, as determined by flow cytometry analysis. Statistical analysis was performed by two-way ANOVA with Bonferroni posttest ( ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, mean ± SEM, n = 3). (b) Cell death mechanisms in con, MCT4, and MCT4 KD F98 cells, as determined by flow cytometry analysis. Viable cells are defined as both PI- and Annexin V-negative, damaged cells are defined as PI-positive and Annexin V-negative, apoptotic cells are defined as PI-negative and Annexin V-positive, and late apoptotic/necrotic cells are defined as both PI- and Annexin V-positive. Statistical analysis was performed by two-way ANOVA with Bonferroni posttest ( ∗∗ p < 0.01; ∗∗∗ p < 0.001, mean ± SEM, n = 3). (c) Ferroptosis in con, MCT4, and MCT4 KD F98 cells treated with 10 μ M erastin and 1 μ M ferrostatin, as determined by MTT assay. Data were normalized to untreated controls. Statistical analysis was performed by one-way ANOVA with Bonferroni posttest ( ns p > 0.05; ∗∗∗ p < 0.001, mean ± SEM, n = 3).

Article Snippet: To assess ferroptosis as described previously [ ], cells were additionally treated with 10 μ M erastin and 1 μ M ferrostatin (both from Sigma Aldrich, Taufkirchen, Germany) per well before culturing.

Techniques: Over Expression, Cell Cycle Assay, Flow Cytometry, MTT Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: lncRNA ZFAS1 Positively Facilitates Endothelial Ferroptosis via miR-7-5p/ACSL4 Axis in Diabetic Retinopathy

doi: 10.1155/2022/9004738

Figure Lengend Snippet: Inhibition of ZFAS1 rescued HG-induced ferroptosis in hRECs. (a) Both apoptosis inhibitor TUDCA and ferroptosis inhibitor Fer-1 administration rescued the downregulated cell viability in HG group. Compared to HG control, there is no difference in total (b) or ferrous iron level (c), lipid hydroperoxide accumulation (d and e), nor GPx4 expression level (f) after 10 μ M apoptosis inhibitor TUDCA, necrosis inhibitor necrostatin-1, pyroptosis inhibitor TETD treatment for 48 h, while transfection of Sh-ZFAS1 remarkably lightened the above ferroptosis phenotypes. n = 5 replicates. P > 0.05. 10 μ M Fer-1 treatment for 48 h notably ameliorated the HG-induced ferroptosis-related phenotypes indicated above. n = 5 replicates. Data are presented as ± SEM. Ns: no significant; ∗∗ P < 0.01 and ∗∗∗ P < 0.001. Scale bar, 50 μ m.

Article Snippet: To detect the role of ferroptotic signals in HG-induced endothelial dysfunction, hRECs were treated with 10 μ M apoptosis inhibitor tauroursodeoxycholic acid (TUDCA) (MCE, 35807-85-3), 10 μ M necrosis inhibitor necrostatin-1 (MCE, 4311-88-0), 10 μ M ferroptosis inhibitor ferrostatin-1 (Fer-1) (MCE, HY-100579), and 10 μ M pyroptosis inhibitor tetraethylthiuram disulfide (TETD) (MCE, 97-77-8) for 48 h.

Techniques: Inhibition, Control, Expressing, Transfection