Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3
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Purpose: In this article, we aimed to investigate the influences of luteolin on inflammatory injury to cardiomyocytes induced bylipopolysaccharide (LPS). Materials and Methods: H9c2 cells were pretreated with different concentrations of luteolin (10, 20, and 50 μM) for 12 h and thenstimulated with 10 μg/mL LPS or no LPS for 6 h. Cell viability was detected by CCK-8 assay. Cell apoptosis was determined byflow cytometry. QRT-PCR and Western blotting were utilized to examine mRNA and protein levels. ELISA was used to determinethe levels of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin (IL)-6, IL-1β, and IL-18 in cell supernatantsamong different groups of H9c2 cells. Immunofluorescence was applied to evaluate reactive oxygen species formation inH9c2 cells. M-mode images of echocardiography, the ejection fraction test, fractional shortening test, end-systolic volume test, andend-diastolic volume test of mouse heart function were obtained by ultrasonic electrocardiogram. Results: Luteolin could alleviate inflammatory damage and inflammatory factor expression among LPS-induced H9c2 cells. Additionally,we found that luteolin decreased LPS-stimulated inflammatory damage in H9c2 cells by down-regulating NOD-likereceptor family pyrin domain containing 3 (Nlrp3). Luteolin also improved myocardial function in mice treated with LPS and reducedmyocardial relaxation. Luteolin reversed myocardial histological abnormalities in mice and reduced inflammation andcardiomyocyte apoptosis. Additionally, luteolin inhibited oxidative stress-mediated myocardial and systemic tissue damage inmice. Finally, luteolin reduced LPS-induced inflammatory damage in mouse cardiomyocytes by down-regulating Nlrp3. Conclusion: We found that luteolin could reduce inflammatory damage to cardiomyocytes induced by LPS by down-regulatingNlrp3.
Abstract
Purpose: In this article, we aimed to investigate the influences of luteolin on inflammatory injury to cardiomyocytes induced bylipopolysaccharide (LPS). Materials and Methods: H9c2 cells were pretreated with different concentrations of luteolin (10, 20, and 50 μM) for 12 h and thenstimulated with 10 μg/mL LPS or no LPS for 6 h. Cell viability was detected by CCK-8 assay. Cell apoptosis was determined byflow cytometry. QRT-PCR and Western blotting were utilized to examine mRNA and protein levels. ELISA was used to determinethe levels of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, interleukin (IL)-6, IL-1β, and IL-18 in cell supernatantsamong different groups of H9c2 cells. Immunofluorescence was applied to evaluate reactive oxygen species formation inH9c2 cells. M-mode images of echocardiography, the ejection fraction test, fractional shortening test, end-systolic volume test, andend-diastolic volume test of mouse heart function were obtained by ultrasonic electrocardiogram. Results: Luteolin could alleviate inflammatory damage and inflammatory factor expression among LPS-induced H9c2 cells. Additionally,we found that luteolin decreased LPS-stimulated inflammatory damage in H9c2 cells by down-regulating NOD-likereceptor family pyrin domain containing 3 (Nlrp3). Luteolin also improved myocardial function in mice treated with LPS and reducedmyocardial relaxation. Luteolin reversed myocardial histological abnormalities in mice and reduced inflammation andcardiomyocyte apoptosis. Additionally, luteolin inhibited oxidative stress-mediated myocardial and systemic tissue damage inmice. Finally, luteolin reduced LPS-induced inflammatory damage in mouse cardiomyocytes by down-regulating Nlrp3. Conclusion: We found that luteolin could reduce inflammatory damage to cardiomyocytes induced by LPS by down-regulatingNlrp3.
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