التفاصيل البيبلوغرافية
| العنوان: |
Polypeptide from Moschus Suppresses Lipopolysaccharide-Induced Inflammation by Inhibiting NF-κ B-ROS/NLRP3 Pathway. |
| المؤلفون: |
Yi, Jing, Li, Li, Yin, Zhu-jun, Quan, Yun-yun, Tan, Rui-rong, Chen, Shi-long, Lang, Ji-rui, Li, Jiao, Zeng, Jin, Li, Yong, Sun, Zi-jian, Zhao, Jun-ning |
| المصدر: |
Chinese Journal of Integrative Medicine; Oct2023, Vol. 29 Issue 10, p895-904, 10p |
| مصطلحات موضوعية: |
INFLAMMATION prevention, LUNG anatomy, PEPTIDE analysis, LIPOPOLYSACCHARIDES, CYTOKINES, FLOW cytometry, IN vitro studies, INTERLEUKINS, HIGH performance liquid chromatography, STAINS & staining (Microscopy), ANTI-inflammatory agents, INFLAMMATION, ANIMAL experimentation, ELECTROPHORESIS, WESTERN immunoblotting, IMMUNOHISTOCHEMISTRY, NF-kappa B, SIGNAL peptides, MACROPHAGES, CELLULAR signal transduction, CELL survival, GENE expression, LACTATE dehydrogenase, ENZYME-linked immunosorbent assay, MESSENGER RNA, MAMMALS, TISSUE extracts, REACTIVE oxygen species, POLYMERASE chain reaction, CELL lines, PEPTIDES, MICE, CHINESE medicine |
| مستخلص: |
Objective: To examine the anti-inflammatory effects and potential mechanisms of polypeptide from Moschus (PPM) in lipopolysaccharide (LPS)-induced THP-1 macrophages and BALB/c mice. Methods: The polypeptide was extracted from Moschus and analyzed by high-performance liquid chromatography and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Subsequently, LPS was used to induce inflammation in THP-1 macrophages and BALB/c mice. In LPS-treated or untreated THP-1 macrophages, cell viability was observed by cell counting kit 8 and lactate dehydrogenase release assays; the proinflammatory cytokines and reactive oxygen species (ROS) were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively; and protein and mRNA levels were measured by Western blot and real-time quantitative polymerase chain reaction (qRT-PCR), respectively. In LPS-induced BALB/c mice, the proinflammatory cytokines were measured, and lung histology and cytokines were observed by hematoxylin and eosin (HE) and immunohistochemical (IHC) staining, respectively. Results: The SDS-PAGE results suggested that the molecular weight of purified PPM was in the range of 10–26 kD. In vitro, PPM reduced the production of interleukin 1β (IL-1β), IL-18, tumor necrosis factor α (TNF-α), IL-6 and ROS in LPS-induced THP-1 macrophages (P<0.01). Western blot analysis demonstrated that PPM inhibited LPS-induced nuclear factor κB (NF-κB) pathway and thioredoxin interacting protein (TXNIP)/nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3) inflammasome pathway by reducing protein expression of phospho-NF-κB p65, phospho-inhibitors of NF-κB (Iκ Bs) kinase α/β (IKKα/β), TXNIP, NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and pro-caspase-1 (P<0.05 or P<0.01). In addition, qRT-PCR revealed the inhibitory effects of PPM on the mRNA levels of TXNIP, NLRP3, ASC, and caspase-1 (P<0.05 or P<0.01). Furthermore, in LPS-induced BALB/c mice, PPM reduced TNF-α and IL-6 levels in serum (P<0.05 or P<0.01), decreased IL-1β and IL-18 levels in the lungs (P<0.01) and alleviated pathological injury to the lungs. Conclusion: PPM could attenuate LPS-induced inflammation by inhibiting the NF-κB-ROS/NLRP3 pathway, and may be a novel potential candidate drug for treating inflammation and inflammation-related diseases. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
