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Sanguinarine Attenuates Lipopolysaccharide-induced Inflammation and Apoptosis by Inhibiting the TLR4/NF-κB Pathway in H9c2 Cardiomyocytes.
Sanguinarine Attenuates Lipopolysaccharide-induced Inflammation and Apoptosis by Inhibiting the TLR4/NF-κB Pathway in H9c2 Cardiomyocytes.
- Source :
-
Current medical science [Curr Med Sci] 2018 Apr; Vol. 38 (2), pp. 204-211. Date of Electronic Publication: 2018 Apr 30. - Publication Year :
- 2018
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Abstract
- The inflammatory response is involved in the pathogenesis of the most common types of heart disease. Sanguinarine (SAN) has various pharmacological properties such as anti-inflammatory, antioxidant, antibacterial, antitumor, and immune-enhancing properties. However, few studies have investigated the effects of SAN on lipopolysaccharide (LPS)-induced inflammatory and apoptotic responses in H9c2 cardiomyocytes. Therefore, in this study, H9c2 cells were co-treated with SAN and LPS, and the mRNA levels of pro-inflammation markers and the apoptosis rate were measured to clarify the effect of SAN on cardiac inflammation. The underlying mechanism was further investigated by detecting the activation of Toll-like receptor (TLR)4/nuclear factor-κB (NF-κB) signaling pathways. As a result, increased mRNA expression of interleukin (IL)-1β, IL-6, and TNFα induced by LPS was attenuated after SAN treatment; LPS-induced apoptosis of H9c2 cardiomyocytes and cleaved-caspase 8, 9, 3 were all significantly reduced by SAN. Further experiments showed that the beneficial effect of SAN on blocking the inflammation and apoptosis of H9c2 cardiomyocytes induced by LPS was associated with suppression of the TLR4/NF-κB signaling pathway. It was suggested that SAN suppressed the LPS-induced inflammation and apoptosis of H9c2 cardiomyocytes, which may be mediated by inhibition of the TLR4/NF-κB signaling pathway. Thus, SAN may be a feasible therapy to treat sepsis patients with cardiac dysfunction.
- Subjects :
- Animals
Benzophenanthridines pharmacology
Caspases genetics
Caspases metabolism
Cell Line
Cell Survival drug effects
Cytokines genetics
Cytokines metabolism
Down-Regulation drug effects
Inflammation Mediators metabolism
Isoquinolines pharmacology
Lipopolysaccharides
Membrane Potential, Mitochondrial drug effects
Models, Biological
Myocytes, Cardiac drug effects
Myocytes, Cardiac pathology
RNA, Messenger genetics
RNA, Messenger metabolism
Rats
Up-Regulation genetics
bcl-2-Associated X Protein genetics
bcl-2-Associated X Protein metabolism
Apoptosis drug effects
Benzophenanthridines therapeutic use
Inflammation chemically induced
Inflammation drug therapy
Isoquinolines therapeutic use
Myocytes, Cardiac metabolism
NF-kappa B metabolism
Signal Transduction drug effects
Toll-Like Receptor 4 metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 2523-899X
- Volume :
- 38
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Current medical science
- Publication Type :
- Academic Journal
- Accession number :
- 30074177
- Full Text :
- https://doi.org/10.1007/s11596-018-1867-4