ferroptosis inhibitor ferrostatin 1  (MedChemExpress)

Journal: Bioactive Materials

Article Title: Spermidine-functionalized Janus hydrogel microneedles inhibit ferroptosis and promote healing of oral ulcers

doi: 10.1016/j.bioactmat.2026.01.016

Figure Lengend Snippet: Evaluation of ferroptosis inhibition, antioxidant, and anti-inflammatory effects of MN-HTSO-C in vitro. (A) Lipid peroxidation analyzed by oxidized-BODIPY flow cytometry (left) and quantification (right) (n = 3). (B) Cell viability assessed by Live/Dead™ staining after treatment with hydrogen peroxide (H 2 O 2 ) in the presence or absence of MN-HTSO-C or Ferrostatin-1 (Fer-1) (n = 3). Scale bar: 100 μm. (C) Quantitative analysis of cell death/live ratios under different treatment conditions (n = 3). (D) Reactive oxygen species ( ROS) (green)/DAPI (blue) immunofluorescence in H 2 O 2 -treated cells with or without MN-HTSO-C (n = 5). Scale bar: 20 μm. (E) Quantification of relative ROS fluorescence intensity (n = 5). (F) Immunofluorescence of inducible nitric oxide synthas (iNOS) and arginase 1 (ARG1) in H 2 O 2 -treated cells with or without MN-HTSO-C (n = 6). Scale bar: 50 μm. Data represent the mean ± SD. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001. Statistical significance was determined by One-way ANOVA test.

Article Snippet: To investigate the involvement of ferroptosis, cells were co-treated with the ferroptosis inhibitor Ferrostatin-1 (Fer-1, HY-100579, MCE) or the ferroptosis inducer RSL-3 (HY-100218 A, MCE), serving as positive and negative controls, respectively, according to the experimental design.

Techniques: Inhibition, In Vitro, Flow Cytometry, Staining, Immunofluorescence, Fluorescence

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Expressing, Western Blot, CCK-8 Assay

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,"ns" P ≥ 0.05.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques:

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Western Blot, Expressing

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Expressing, Western Blot, CCK-8 Assay

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,"ns" P ≥ 0.05.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques:

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Western Blot, Expressing