Effect of Sulforaphane on cardiac injury induced by sepsis in a mouse model : Role of toll-like receptor 4
©2023 JOURNAL of MEDICINE and LIFE..
As sepsis is associated with a 50% increase in mortality, sepsis-induced cardiomyopathy has become a critical topic. A multidisciplinary approach is required for the diagnosis and treatment of septic cardiomyopathy. This study looked at Sulforaphane, a natural product that aims to evaluate cardiac function after sepsis, and its likely mechanism of action. Twenty-four adult male Swiss albino mice were randomly divided into 4 equal groups (n=6): sham, CLP, vehicle Sulforaphane (the same amount of DMSO injected IP one hour before the CLP), and Sulforaphane group (one hour before the CLP, a 5mg/kg dose of Sulforaphane was injected). Cardiac tissue levels of toll-like receptor 4 (TLR-4), pro-inflammatory mediators, anti-inflammatory markers, oxidative stress markers, apoptosis markers, and serum cardiac damage biomarkers were assessed using ELISA. Statistical analyses, including t-tests and ANOVA tests, were performed with a significance level of 0.05 for normally distributed data. Compared to the sham group, the sepsis group had significantly elevated levels of TLR-4, IL-6, TNF-α, MIF, F2-isoprostane, caspase-3, cTn-I, and CK-MB (p<0.05). In contrast, the Sulforaphane pre-treated group demonstrated significantly lower levels of these markers (p<0.05). Additionally, Bcl-2 levels were significantly reduced (p<0.05) in the Sulforaphane group. Sulforaphane administration also significantly attenuated cardiac tissue injury (p<0.05). The findings suggest that Sulforaphane can decrease heart damage in male mice during CLP-induced polymicrobial sepsis by suppressing TLR-4/NF-kB downstream signal transduction pathways.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:16 |
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| Enthalten in: |
Journal of medicine and life - 16(2023), 7 vom: 07. Juli, Seite 1120-1126 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Hadi, Sarah Mohammed Hussain [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 31.10.2023 Date Revised 31.10.2023 published: Print Citation Status MEDLINE |
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| doi: |
10.25122/jml-2023-0015 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM363920897 |
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| 100 | 1 | |a Hadi, Sarah Mohammed Hussain |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effect of Sulforaphane on cardiac injury induced by sepsis in a mouse model |b Role of toll-like receptor 4 |
| 264 | 1 | |c 2023 | |
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| 500 | |a Date Completed 31.10.2023 | ||
| 500 | |a Date Revised 31.10.2023 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a ©2023 JOURNAL of MEDICINE and LIFE. | ||
| 520 | |a As sepsis is associated with a 50% increase in mortality, sepsis-induced cardiomyopathy has become a critical topic. A multidisciplinary approach is required for the diagnosis and treatment of septic cardiomyopathy. This study looked at Sulforaphane, a natural product that aims to evaluate cardiac function after sepsis, and its likely mechanism of action. Twenty-four adult male Swiss albino mice were randomly divided into 4 equal groups (n=6): sham, CLP, vehicle Sulforaphane (the same amount of DMSO injected IP one hour before the CLP), and Sulforaphane group (one hour before the CLP, a 5mg/kg dose of Sulforaphane was injected). Cardiac tissue levels of toll-like receptor 4 (TLR-4), pro-inflammatory mediators, anti-inflammatory markers, oxidative stress markers, apoptosis markers, and serum cardiac damage biomarkers were assessed using ELISA. Statistical analyses, including t-tests and ANOVA tests, were performed with a significance level of 0.05 for normally distributed data. Compared to the sham group, the sepsis group had significantly elevated levels of TLR-4, IL-6, TNF-α, MIF, F2-isoprostane, caspase-3, cTn-I, and CK-MB (p<0.05). In contrast, the Sulforaphane pre-treated group demonstrated significantly lower levels of these markers (p<0.05). Additionally, Bcl-2 levels were significantly reduced (p<0.05) in the Sulforaphane group. Sulforaphane administration also significantly attenuated cardiac tissue injury (p<0.05). The findings suggest that Sulforaphane can decrease heart damage in male mice during CLP-induced polymicrobial sepsis by suppressing TLR-4/NF-kB downstream signal transduction pathways | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a ANOVA: Analysis of Variance | |
| 650 | 4 | |a AP-1: Activator protein 1 | |
| 650 | 4 | |a Bcl-2: B-cell lymphoma 2 | |
| 650 | 4 | |a CK-MB: creatinine kinase MB | |
| 650 | 4 | |a CLP | |
| 650 | 4 | |a CLP: Cecal Ligation And Puncture | |
| 650 | 4 | |a DMSO-Dimethyl Sulfoxide | |
| 650 | 4 | |a ELISA: enzyme-linked immunosorbent assay | |
| 650 | 4 | |a ERK: Extracellular signal-regulated kinase | |
| 650 | 4 | |a IL-10: Interleukin 10 | |
| 650 | 4 | |a IL-6: Interleukin 6 | |
| 650 | 4 | |a IP: intraperitoneally | |
| 650 | 4 | |a JNK: c-Jun N-terminal kinase | |
| 650 | 4 | |a KEAP-1: Kelch-like ECH-associated protein 1 | |
| 650 | 4 | |a LPS: lipopolysaccharide | |
| 650 | 4 | |a MAPK: Mitogen-Activated Protein Kinase | |
| 650 | 4 | |a MD-2: Myeloid differentiation factor-2 | |
| 650 | 4 | |a MIF: Macrophage migration inhibitory | |
| 650 | 4 | |a NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells | |
| 650 | 4 | |a Nrf2: nuclear factor erythroid 2-related factor 2 | |
| 650 | 4 | |a Oxidative stress | |
| 650 | 4 | |a ROS: reactive oxygen species | |
| 650 | 4 | |a Sulforaphane | |
| 650 | 4 | |a TLR- 4/NF- kB signaling pathways | |
| 650 | 4 | |a TLR4: Toll-like receptor 4 | |
| 650 | 4 | |a TNF- α: Tumor necrosis factor alpha | |
| 650 | 4 | |a cTn-I: cardiac troponin I | |
| 650 | 4 | |a cytokines | |
| 650 | 4 | |a sepsis | |
| 650 | 4 | |a °C: Celsius Degree | |
| 650 | 7 | |a Toll-Like Receptor 4 |2 NLM | |
| 650 | 7 | |a sulforaphane |2 NLM | |
| 650 | 7 | |a GA49J4310U |2 NLM | |
| 700 | 1 | |a Majeed, Sahar |e verfasserin |4 aut | |
| 700 | 1 | |a Ghafil, Fadhaa Abdulameer |e verfasserin |4 aut | |
| 700 | 1 | |a Altoraihi, Kaswer |e verfasserin |4 aut | |
| 700 | 1 | |a Hadi, Najah Rayish |e verfasserin |4 aut | |
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| 773 | 1 | 8 | |g volume:16 |g year:2023 |g number:7 |g day:07 |g month:07 |g pages:1120-1126 |
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