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We began analyzing https://cardiothoracicsurgery.biomedcentral.com/articles/10.1186/s13019-025-03366-1, but it redirected us to https://cardiothoracicsurgery.biomedcentral.com/articles/10.1186/s13019-025-03366-1. The analysis below is for the second page.

Title[redir]:
Inhibition of mir-155-5p alleviates cardiomyocyte pyroptosis induced by hypoxia/reoxygenation via targeting SIRT1-mediated activation of the NLRP3 inflammasome | Journal of Cardiothoracic Surgery | Full Text
Description:
Objective The hypoxia/reoxygenation (H/R)-induced pyroptosis of cardiomyocytes plays a crucial role in the pathogenesis of myocardial infarction (MI). miR-155-5p represents a promising target for MI therapy. However, its involvement in H/R-induced pyroptosis remains unclear. Methods The H/R exposed rat cardiomyocyte H9c2 was utilized as in vitro model, and the expression levels of miR-155-5p and SIRT1 in cells were modulated through cell transfection experiments. Cell proliferative activity was assessed using the Cell counting kit-8 assay. Supernatant lactate dehydrogenase (LDH) activity was determined through colorimetry. The levels of living and dead cell were observed via Calcin-AM/PI staining. Levels of supernatant interleukin (IL)-1β and IL-18 were measured using ELISA assay. The expression levels of miR-155-5p and silent information regulator 1 (SIRT1) mRNA were detected by qRT-PCR. The protein expression levels of SIRT1, NLRP3, N-terminal gasdermin D (GSDMD-N), and Cleaved caspase-1 were evaluated using Western blot analysis. The targeted regulatory relationship between miR-155-5p and SIRT1 was verified using dual luciferase reporter gene assay. Results The proliferation activity of H9c2 cells induced by H/R was attenuated, accompanied by severe injury, increased cell death, and the release of a substantial amount of pro-inflammatory cytokines IL-1β and IL-18. In addition, H/R stimulation resulted in the upregulation of miR-155-5p expression and downregulation of SIRT1 expression in H9c2 cells. Suppression of miR-155-5p or overexpression of SIRT1 exhibited ameliorative effects on H/R-induced cellular injury in H9c2 cells and inhibited NLRP3 inflammasome-mediated pyroptosis. The dual-luciferase assay confirmed the direct targeting of SIRT1 by miR-155-5p in H9c2 cells. Furthermore, partial reversal of the inhibitory effect of miR-155-5p inhibitor on H/R-induced NLRP3 inflammasome-mediated pyroptosis in H9c2 cells was observed upon interference with SIRT1 expression. Conclusion Inhibition of miR-155-5p alleviates cardiomyocyte pyroptosis induced by H/R via targeting SIRT1-mediated activation of the NLRP3 inflammasome.

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Keywords {🔍}

cells, mirp, sirt, pyroptosis, pubmed, myocardial, nlrp, cell, article, expression, google, scholar, injury, levels, inflammasome, cas, fig, inhibition, protein, death, cardiomyocyte, central, activity, assay, activation, cardiomyocytes, inhibitor, hrinduced, level, induced, targeting, supernatant, analysis, infarction, wang, ldh, ilβ, western, blot, cardiac, inflammatory, demonstrated, china, overexpression, study, exposure, observed, gsdmdn, significant, data,

Topics {✒️}

tlr4/nf-κb p65 pathway springer nature p53/mir-155-5p/sirt1 loop additional information publisher induced nlrp3-mediated pyroptosis post-myocardial infarction remodelling nlrp3 inflammasome-mediated pyroptosis pro-inflammatory cytokines il-1β sirt1/nf-κb pathway hypoxic-ischemic brain damage visualized figures mir-665/mef2d/nrf2 axis myocardial ischemia-reperfusion injury myocardial ischemia/reperfusion injury mir-155-5p promotes pyroptosis /r-induced cellular injury references peng post-myocardial infarction patients post-resuscitation cardiac dysfunction hypoxic-ischemic brain injury dual-lucy assay kit pyroptosis-inducing cancer drugs author information authors release pro-inflammatory cytokines /r-induced h9c2 cells si-sirt1 effectively counteracted downregulated mir-155-5p expression mir-155-5p effectively attenuated mir-155-5p/sirt1 axis materials independent sample t-test sharing /r-exposed h9c2 cells c-terminal domain connected /r-induced damage cardiomyocyte pyroptosis induced mir-155-5p regulates pyroptosis methods cell culture privacy choices/manage cookies dual-luciferase assay confirmed targeting sirt1-mediated activation acute myocardial infarction authors scientific editing results pyroptosis mediated /r-induced pyroptosis data availability state privacy rights mir-155-5p inhibitor resulted bmc induced cardiomyocyte apoptosis

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         description:The hypoxia/reoxygenation (H/R)-induced pyroptosis of cardiomyocytes plays a crucial role in the pathogenesis of myocardial infarction (MI). miR-155-5p represents a promising target for MI therapy. However, its involvement in H/R-induced pyroptosis remains unclear. The H/R exposed rat cardiomyocyte H9c2 was utilized as in vitro model, and the expression levels of miR-155-5p and SIRT1 in cells were modulated through cell transfection experiments. Cell proliferative activity was assessed using the Cell counting kit-8 assay. Supernatant lactate dehydrogenase (LDH) activity was determined through colorimetry. The levels of living and dead cell were observed via Calcin-AM/PI staining. Levels of supernatant interleukin (IL)-1β and IL-18 were measured using ELISA assay. The expression levels of miR-155-5p and silent information regulator 1 (SIRT1) mRNA were detected by qRT-PCR. The protein expression levels of SIRT1, NLRP3, N-terminal gasdermin D (GSDMD-N), and Cleaved caspase-1 were evaluated using Western blot analysis. The targeted regulatory relationship between miR-155-5p and SIRT1 was verified using dual luciferase reporter gene assay. The proliferation activity of H9c2 cells induced by H/R was attenuated, accompanied by severe injury, increased cell death, and the release of a substantial amount of pro-inflammatory cytokines IL-1β and IL-18. In addition, H/R stimulation resulted in the upregulation of miR-155-5p expression and downregulation of SIRT1 expression in H9c2 cells. Suppression of miR-155-5p or overexpression of SIRT1 exhibited ameliorative effects on H/R-induced cellular injury in H9c2 cells and inhibited NLRP3 inflammasome-mediated pyroptosis. The dual-luciferase assay confirmed the direct targeting of SIRT1 by miR-155-5p in H9c2 cells. Furthermore, partial reversal of the inhibitory effect of miR-155-5p inhibitor on H/R-induced NLRP3 inflammasome-mediated pyroptosis in H9c2 cells was observed upon interference with SIRT1 expression. Inhibition of miR-155-5p alleviates cardiomyocyte pyroptosis induced by H/R via targeting SIRT1-mediated activation of the NLRP3 inflammasome.
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      description:The hypoxia/reoxygenation (H/R)-induced pyroptosis of cardiomyocytes plays a crucial role in the pathogenesis of myocardial infarction (MI). miR-155-5p represents a promising target for MI therapy. However, its involvement in H/R-induced pyroptosis remains unclear. The H/R exposed rat cardiomyocyte H9c2 was utilized as in vitro model, and the expression levels of miR-155-5p and SIRT1 in cells were modulated through cell transfection experiments. Cell proliferative activity was assessed using the Cell counting kit-8 assay. Supernatant lactate dehydrogenase (LDH) activity was determined through colorimetry. The levels of living and dead cell were observed via Calcin-AM/PI staining. Levels of supernatant interleukin (IL)-1β and IL-18 were measured using ELISA assay. The expression levels of miR-155-5p and silent information regulator 1 (SIRT1) mRNA were detected by qRT-PCR. The protein expression levels of SIRT1, NLRP3, N-terminal gasdermin D (GSDMD-N), and Cleaved caspase-1 were evaluated using Western blot analysis. The targeted regulatory relationship between miR-155-5p and SIRT1 was verified using dual luciferase reporter gene assay. The proliferation activity of H9c2 cells induced by H/R was attenuated, accompanied by severe injury, increased cell death, and the release of a substantial amount of pro-inflammatory cytokines IL-1β and IL-18. In addition, H/R stimulation resulted in the upregulation of miR-155-5p expression and downregulation of SIRT1 expression in H9c2 cells. Suppression of miR-155-5p or overexpression of SIRT1 exhibited ameliorative effects on H/R-induced cellular injury in H9c2 cells and inhibited NLRP3 inflammasome-mediated pyroptosis. The dual-luciferase assay confirmed the direct targeting of SIRT1 by miR-155-5p in H9c2 cells. Furthermore, partial reversal of the inhibitory effect of miR-155-5p inhibitor on H/R-induced NLRP3 inflammasome-mediated pyroptosis in H9c2 cells was observed upon interference with SIRT1 expression. Inhibition of miR-155-5p alleviates cardiomyocyte pyroptosis induced by H/R via targeting SIRT1-mediated activation of the NLRP3 inflammasome.
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