Zanthoxylum bungeanum Seed Oil Attenuates LPS-Induced BEAS-2B Cell Activation and Inflammation by Inhibiting the TLR4/MyD88/NF-κB Signaling Pathway
Autor: | Jing Hou, Jianping Gao, Yuan-jing Niu, Xiao-ting Zhang, Jiangtao Zhou, Jingyi Meng, Yun'e Bai, Jun Wang |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
medicine.diagnostic_test
Article Subject Chemistry Monocyte Inflammation medicine.disease_cause Molecular biology Proinflammatory cytokine Other systems of medicine medicine.anatomical_structure Complementary and alternative medicine Western blot medicine TLR4 Tumor necrosis factor alpha medicine.symptom Cell activation Oxidative stress RZ201-999 Research Article |
Zdroj: | Evidence-based Complementary and Alternative Medicine : eCAM Evidence-Based Complementary and Alternative Medicine, Vol 2021 (2021) |
ISSN: | 1741-427X |
DOI: | 10.1155/2021/2073296 |
Popis: | Background. Zanthoxylum bungeanum seed oil (ZBSO) is a natural essential oil derived from the seeds of the Chinese medicinal plant Zanthoxylum bungeanum, which has been investigated for antitumor and anti-inflammatory effects. However, little is known regarding the effects of ZBSO in chronic obstructive pulmonary disease (COPD). Methods. In this study, lung epithelial cells (BEAS-2B) were induced by lipopolysaccharide (LPS) to establish an in vitro model of COPD, and cytotoxicity was detected by a cell counting kit 8 (CCK-8) assay. Griess test, enzyme-linked immunosorbent assay (ELISA), reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), western blot, immunofluorescence, and molecular docking analyses were used to investigate the effects of ZBSO and its potential mechanisms. Results. The results showed that LPS promoted the expression of nitric oxide (NO), reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-2 (MMP-2), MMP-9, cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2), suggesting that LPS can induce inflammation and oxidative stress in BEAS-2B cells. ZBSO inhibits the LPS-induced expression of inflammatory mediators and proinflammatory cytokines in BEAS-2B cells. The molecular docking results indicated that active components in ZBSO could successfully dock with toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and p65. Immunofluorescence and western blot analyses further demonstrated that ZBSO repressed protein expression associated with the TLR4/MyD88/nuclear factor-κB (NF-κB) signaling pathway. Conclusions. ZBSO reduced the inflammatory response and oxidative stress induced by LPS by inhibiting the TLR4/MyD88/NF-κB signaling pathway, thereby suppressing COPD. ZBSO may represent a promising therapeutic candidate for COPD treatment. |
Databáze: | OpenAIRE |
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