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SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and <t>eNOS</t> expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.
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SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and <t>eNOS</t> expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.
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SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and <t>eNOS</t> expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.
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inducible nitric oxide synthase  (Bioss)
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SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and <t>eNOS</t> expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.
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SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and eNOS expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.

Journal: Journal of Lipid Research

Article Title: S-nitrosylation contributes to ER stress and aggresome formation in secosterol-B-mediated endothelial dysfunction

doi: 10.1016/j.jlr.2026.101017

Figure Lengend Snippet: SEC-B induces NSS through increased intracellular NO and RNS and depletion of the antioxidant GSH. Quantitative analysis of RNS (A), GSH (B), and NO (C) levels in HUVECs treated with 10 μM SEC-B. Data are expressed as the mean ± SD of the values obtained from at least three independent experiments.∗ P < 0.05, ∗∗ P < 0.01 versus untreated cells. D: Confocal microscopy of 4,5-diaminofluorescein diacetate-stained HUVECs after 24 h of treatment with 10 μM SEC-B. The scale bar represents 20 μm. E and F: Western immunoblotting analysis and quantitation of iNOS and eNOS expression levels in HUVECs treated with 10 μM SEC-B. Data are reported in the graph as fold change versus untreated cells. Data are expressed as the mean ± SD of the values obtained from at least four independent experiments. ∗ P < 0.05 versus untreated cells.

Article Snippet: Blots were probed with the following antibodies: anti-spliced X-box binding protein 1 (XBP-1s) (E9V3E, #40435), ATF6 (D4Z8V, #65880), BiP/GRP78 (C50B12, #3177), and protein disulfide isomerase (PDI) (#2446) from Cell Signaling Technology; anti-endothelial NOS (eNOS) (A1548) from ABclonal; and anti-NOS2 (N-20, sc-651) from Santa Cruz Biotechnology.

Techniques: Confocal Microscopy, Staining, Western Blot, Quantitation Assay, Expressing