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(A) Experimental scheme of Langendorff ex vivo mouse hearts perfused with 0 mM NAM (control) or 100 mM NAM-supplemented buffer. (B) Representative electrocardiogram (ECG) shows that acute perfusion with 100 mM NAM rapidly induced VF, contractile dysfunction, and eventually led to cardiac arrest (n=4 males, 2 females). (C) Representiative blots and (D) quantification of acetylated <t>SERCA2a</t> levels of left venticular tissue from control and 100 mM NAM-perfused ex vivo mouse hearts (n=3). Data are expressed as mean ± standard error of the mean. Two tailed unpaired Student t-test was used.
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(A) Experimental scheme of Langendorff ex vivo mouse hearts perfused with 0 mM NAM (control) or 100 mM NAM-supplemented buffer. (B) Representative electrocardiogram (ECG) shows that acute perfusion with 100 mM NAM rapidly induced VF, contractile dysfunction, and eventually led to cardiac arrest (n=4 males, 2 females). (C) Representiative blots and (D) quantification of acetylated <t>SERCA2a</t> levels of left venticular tissue from control and 100 mM NAM-perfused ex vivo mouse hearts (n=3). Data are expressed as mean ± standard error of the mean. Two tailed unpaired Student t-test was used.
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Fig. 7 AEOL treatment enhances <t>SERCA2a</t> activity by upregulating DWORF expression. Maximal SERCA2a activity in the infarct border zone of wild type and Nrf2-KO mice subjected to mI/R, treated as indicated with AEOL and DWORF 15 min after reperfusion onset, and sacrificed at 24 h post-mI/R. Data were obtained from n = 7 mice/group and are presented as mean values ± SEM. ***p < 0.001, determined by one-way ANOVA followed by post hoc Bonferroni correction. Abbreviations are defined in the abbreviations list
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Fig. 7 AEOL treatment enhances <t>SERCA2a</t> activity by upregulating DWORF expression. Maximal SERCA2a activity in the infarct border zone of wild type and Nrf2-KO mice subjected to mI/R, treated as indicated with AEOL and DWORF 15 min after reperfusion onset, and sacrificed at 24 h post-mI/R. Data were obtained from n = 7 mice/group and are presented as mean values ± SEM. ***p < 0.001, determined by one-way ANOVA followed by post hoc Bonferroni correction. Abbreviations are defined in the abbreviations list
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(A) Experimental scheme of Langendorff ex vivo mouse hearts perfused with 0 mM NAM (control) or 100 mM NAM-supplemented buffer. (B) Representative electrocardiogram (ECG) shows that acute perfusion with 100 mM NAM rapidly induced VF, contractile dysfunction, and eventually led to cardiac arrest (n=4 males, 2 females). (C) Representiative blots and (D) quantification of acetylated SERCA2a levels of left venticular tissue from control and 100 mM NAM-perfused ex vivo mouse hearts (n=3). Data are expressed as mean ± standard error of the mean. Two tailed unpaired Student t-test was used.

Journal: bioRxiv

Article Title: Dual effects of nicotinamide on aging-related arrhythmia: protective at low dose, proarrhythmic at high doses

doi: 10.1101/2025.09.22.677785

Figure Lengend Snippet: (A) Experimental scheme of Langendorff ex vivo mouse hearts perfused with 0 mM NAM (control) or 100 mM NAM-supplemented buffer. (B) Representative electrocardiogram (ECG) shows that acute perfusion with 100 mM NAM rapidly induced VF, contractile dysfunction, and eventually led to cardiac arrest (n=4 males, 2 females). (C) Representiative blots and (D) quantification of acetylated SERCA2a levels of left venticular tissue from control and 100 mM NAM-perfused ex vivo mouse hearts (n=3). Data are expressed as mean ± standard error of the mean. Two tailed unpaired Student t-test was used.

Article Snippet: The membrane was then blocked with Intercept Blocking Buffer (927-60001, LI-COR) for 1 h at RT, and incubated with primary antibodies against SERCA2a (1:1000 dilution, 4388, cell signaling), and Pan Acetylation (1:2000 dilution, 66289-1-Ig, Proteintech) overnight at 4°C.

Techniques: Ex Vivo, Control, Two Tailed Test

Fig. 7 AEOL treatment enhances SERCA2a activity by upregulating DWORF expression. Maximal SERCA2a activity in the infarct border zone of wild type and Nrf2-KO mice subjected to mI/R, treated as indicated with AEOL and DWORF 15 min after reperfusion onset, and sacrificed at 24 h post-mI/R. Data were obtained from n = 7 mice/group and are presented as mean values ± SEM. ***p < 0.001, determined by one-way ANOVA followed by post hoc Bonferroni correction. Abbreviations are defined in the abbreviations list

Journal: Molecular medicine (Cambridge, Mass.)

Article Title: AEOL-induced NRF2 activation and DWORF overexpression mitigate myocardial I/R injury.

doi: 10.1186/s10020-025-01242-1

Figure Lengend Snippet: Fig. 7 AEOL treatment enhances SERCA2a activity by upregulating DWORF expression. Maximal SERCA2a activity in the infarct border zone of wild type and Nrf2-KO mice subjected to mI/R, treated as indicated with AEOL and DWORF 15 min after reperfusion onset, and sacrificed at 24 h post-mI/R. Data were obtained from n = 7 mice/group and are presented as mean values ± SEM. ***p < 0.001, determined by one-way ANOVA followed by post hoc Bonferroni correction. Abbreviations are defined in the abbreviations list

Article Snippet: To elute antigen–antibody complexes, the beads were resuspended in 25 μL SDS gel-loading buffer and heated at 95 °C for 4 min. After this, samples were separated by SDSPAGE at 30 mA constant current for 2 h. Immunocomplexes were analyzed by western blotting with primary antibodies to SERCA2a (Cell Signaling, 4388, 1:1000), PLN (Badrilla, A010-14, 1:10,000), or DWORF (Mybiosource, MBS5400388, 1:5000).

Techniques: Activity Assay, Expressing