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scd1  (Proteintech)
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Vitamin A and its metabolites inhibit ferroptosis independent of antioxidant capacity or RAR/RXR activation. (A) Illustration of the structures of VA and ATRA. (B) Measurement of the EC 50 values of VA and ATRA towards RSL3 (0.5 μmol/L) or Erastin (10 μmol/L) induced ferroptosis in HT-1080 cells. Cells were treated with drugs for 24 h. (C) RAL suppressed RSL3 and Erastin-induced ferroptosis in HT-1080 cells. (D) Viability of HT-1080 GPX4 -KO cells treated with the indicated compounds for 24 h after withdrawal of Fer-1, which is essential for the survival of GPX4 -KO cells. (E) The antioxidative capacity of VA (50 μmol/L), ATRA (50 μmol/L) and RAL (50 μmol/L) was analyzed by the DPPH (2,2-diphenyl-1-picrylhydrazyl) assay. Trolox (50 μmol/L) was used as a positive control. (F) The effect of VA, ATRA and RAL on the autoxidation of C11 BODIPY 581/591 initiated by AAPH in EggPC liposomes was measured by FENIX assay. Fer-1 was used as a positive control. (G) Protein expression levels of GPX4, SLC7A11, ACSL4, <t>SCD1,</t> FSP1, HO-1 and NRF2 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (H) Protein expression levels of IRP1, TFRC and FTH1 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (I, J) Cell viability of HT-1080 cells after co-treatment with RSL3 and VA or ATRA in the presence of pan-RAR antagonist AGN193109 (20 μmol/L) (I) or pan-RXR antagonist HX531 (20 μmol/L) (J). (K) The protective effects of VA or ATRA on RSL3-induced ferroptosis in RXRA and RXRB knockout HT-1080 cells. (L) Viability of HT-1080 cells treated with different doses of RAR agonists Ch55 and Adapalene (ADA) under RSL3 (0.5 μmol/L) and Erastin (10 μmol/L)-induced ferroptosis for 24 h. Data shown represent the mean ± SD ( n = 3). ∗∗ P < 0.01, and ∗∗∗ P < 0.001, indicating significant differences between groups. ns means no significance.
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Vitamin A and its metabolites inhibit ferroptosis independent of antioxidant capacity or RAR/RXR activation. (A) Illustration of the structures of VA and ATRA. (B) Measurement of the EC 50 values of VA and ATRA towards RSL3 (0.5 μmol/L) or Erastin (10 μmol/L) induced ferroptosis in HT-1080 cells. Cells were treated with drugs for 24 h. (C) RAL suppressed RSL3 and Erastin-induced ferroptosis in HT-1080 cells. (D) Viability of HT-1080 GPX4 -KO cells treated with the indicated compounds for 24 h after withdrawal of Fer-1, which is essential for the survival of GPX4 -KO cells. (E) The antioxidative capacity of VA (50 μmol/L), ATRA (50 μmol/L) and RAL (50 μmol/L) was analyzed by the DPPH (2,2-diphenyl-1-picrylhydrazyl) assay. Trolox (50 μmol/L) was used as a positive control. (F) The effect of VA, ATRA and RAL on the autoxidation of C11 BODIPY 581/591 initiated by AAPH in EggPC liposomes was measured by FENIX assay. Fer-1 was used as a positive control. (G) Protein expression levels of GPX4, SLC7A11, ACSL4, SCD1, FSP1, HO-1 and NRF2 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (H) Protein expression levels of IRP1, TFRC and FTH1 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (I, J) Cell viability of HT-1080 cells after co-treatment with RSL3 and VA or ATRA in the presence of pan-RAR antagonist AGN193109 (20 μmol/L) (I) or pan-RXR antagonist HX531 (20 μmol/L) (J). (K) The protective effects of VA or ATRA on RSL3-induced ferroptosis in RXRA and RXRB knockout HT-1080 cells. (L) Viability of HT-1080 cells treated with different doses of RAR agonists Ch55 and Adapalene (ADA) under RSL3 (0.5 μmol/L) and Erastin (10 μmol/L)-induced ferroptosis for 24 h. Data shown represent the mean ± SD ( n = 3). ∗∗ P < 0.01, and ∗∗∗ P < 0.001, indicating significant differences between groups. ns means no significance.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Vitamin A and its analogues modulate MUFAs metabolism to improve ferroptosis and aging by direct targeting of ACSL3

doi: 10.1016/j.apsb.2025.11.004

Figure Lengend Snippet: Vitamin A and its metabolites inhibit ferroptosis independent of antioxidant capacity or RAR/RXR activation. (A) Illustration of the structures of VA and ATRA. (B) Measurement of the EC 50 values of VA and ATRA towards RSL3 (0.5 μmol/L) or Erastin (10 μmol/L) induced ferroptosis in HT-1080 cells. Cells were treated with drugs for 24 h. (C) RAL suppressed RSL3 and Erastin-induced ferroptosis in HT-1080 cells. (D) Viability of HT-1080 GPX4 -KO cells treated with the indicated compounds for 24 h after withdrawal of Fer-1, which is essential for the survival of GPX4 -KO cells. (E) The antioxidative capacity of VA (50 μmol/L), ATRA (50 μmol/L) and RAL (50 μmol/L) was analyzed by the DPPH (2,2-diphenyl-1-picrylhydrazyl) assay. Trolox (50 μmol/L) was used as a positive control. (F) The effect of VA, ATRA and RAL on the autoxidation of C11 BODIPY 581/591 initiated by AAPH in EggPC liposomes was measured by FENIX assay. Fer-1 was used as a positive control. (G) Protein expression levels of GPX4, SLC7A11, ACSL4, SCD1, FSP1, HO-1 and NRF2 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (H) Protein expression levels of IRP1, TFRC and FTH1 in HT-1080 cells were analyzed by Western blot. Cells were treated with VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of RSL3 (0.25 μmol/L) for 2.5 h or Erastin (10 μmol/L) for 8 h. (I, J) Cell viability of HT-1080 cells after co-treatment with RSL3 and VA or ATRA in the presence of pan-RAR antagonist AGN193109 (20 μmol/L) (I) or pan-RXR antagonist HX531 (20 μmol/L) (J). (K) The protective effects of VA or ATRA on RSL3-induced ferroptosis in RXRA and RXRB knockout HT-1080 cells. (L) Viability of HT-1080 cells treated with different doses of RAR agonists Ch55 and Adapalene (ADA) under RSL3 (0.5 μmol/L) and Erastin (10 μmol/L)-induced ferroptosis for 24 h. Data shown represent the mean ± SD ( n = 3). ∗∗ P < 0.01, and ∗∗∗ P < 0.001, indicating significant differences between groups. ns means no significance.

Article Snippet: Primary antibodies used were as follows: ACSL3 (Santa Cruz, sc-166374), ACSL3 (Proteintech, 20710-1-AP), ACSL4 (Proteintech, 66617-1-Ig), SLC7A11 (CST, 12691S), GPX4 (HuaBio, ER1803-15), IRP1 (CST, 20272S), TFRC (CST, 13113S), FTH1 (CST, 4393S), RXRA/RXRB (CST, 8589), SCD1 (Proteintech, 28678-1-AP), FSP1 (Proteintech, 20886-1-AP), HSP90 (Proteintech, 13171-1-AP), β -actin (Proteintech, 81115-1-RR) and Vinculin (Sigma, V9131).

Techniques: Activation Assay, Positive Control, Liposomes, Expressing, Western Blot, Knock-Out

VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Vitamin A and its analogues modulate MUFAs metabolism to improve ferroptosis and aging by direct targeting of ACSL3

doi: 10.1016/j.apsb.2025.11.004

Figure Lengend Snippet: VA analogues inhibit ferroptosis through the regulation of MUFA metabolism. (A, B) Lipidomic analysis of MUFAs and PUFAs in membrane lipids including PE (A) and PC (B) following VA (5 μmol/L) and D3 (5 μmol/L) treatment for 12 h in HT-1080 cells. (C) Viability HT-1080 cells treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L) or ATRA (10 μmol/L) in the presence or absence of SCD1 inhibitor A939572 (20 μmol/L) for 24 h. (D) Validation of SCD1 KO in HT-1080 cells. (E) The levels of OA-CoA were decreased in SCD1 knockout HT-1080 cells. (F) Viability of Vector and SCD1 KO cells treated with RSL3 for 24 h. (G) SCD1 KO compromised the anti-ferroptotic effect of VA analogues in HT-1080 cells. Cells were treated with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. (H, I) Supplement of OA restored the protective effect of VA analogues against ferroptosis. Vector and SCD1 KO HT-1080 cells were pretreated with OA in (10 and 20 μmol/L in panel H, and 10 μmol/L in panel I, followed by treatment with RSL3 (0.5 μmol/L) and VA (1 μmol/L), ATRA (10 μmol/L) or D3 (5 μmol/L) for 24 h. All the data are presented as the mean ± SD ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, indicating significant differences between groups.

Article Snippet: Primary antibodies used were as follows: ACSL3 (Santa Cruz, sc-166374), ACSL3 (Proteintech, 20710-1-AP), ACSL4 (Proteintech, 66617-1-Ig), SLC7A11 (CST, 12691S), GPX4 (HuaBio, ER1803-15), IRP1 (CST, 20272S), TFRC (CST, 13113S), FTH1 (CST, 4393S), RXRA/RXRB (CST, 8589), SCD1 (Proteintech, 28678-1-AP), FSP1 (Proteintech, 20886-1-AP), HSP90 (Proteintech, 13171-1-AP), β -actin (Proteintech, 81115-1-RR) and Vinculin (Sigma, V9131).

Techniques: Analogues, Membrane, Biomarker Discovery, Knock-Out, Plasmid Preparation