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      Inhibitory Effect of Phellinus baumii Extract on CFA-Induced Inflammation in MH-S Cells through Nuclear Factor- κB and Mitogen-Activated Protein Kinase Signaling Pathways

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          Abstract

          Phellinus baumii is a mushroom utilized as a traditional medicine for a wide range of human ailments, including diabetes, hypertension, hypercholesterolemia, and cancer, in Asia. The purpose of this study was to find out whether Phellinus baumii extract (PBE) could reduce inflammation caused by coal fly ash (CFA) in alveolar macrophages (MH-S). The anti-inflammatory effect of PBE was evaluated by measuring the nitric oxide (NO) concentration after the onset of CFA-stimulated inflammation in MH-S cells. Polymerase chain reaction (PCR) was used to examine inflammatory gene expression. Western blotting and immunofluorescence (IF) studies were used to investigate the inflammatory mechanism in MH-S cells. According to our results, the PBE suppressed CFA-induced NO generation in the MH-S cells dose-dependently. Furthermore, PBE inhibited the proinflammatory mediators and cytokines generated by exposure to CFA, including cyclooxygenase 2 (COX-2) and inducible NO synthase (iNOS), interleukin (IL)-1 β, IL-6, and tumor necrosis factor-alpha (TNF- α). Real-time PCR was also used to determine the inhibiting effect of the PBE on proinflammatory factors such as COX-2, iNOS, IL-1 β, IL-6, and TNF- α. Moreover, Western blot was used to assess the effects of the PBE on the nuclear factor-kappa B (NF- κB) and mitogen-activated protein kinase (MAPK) pathways in the CFA-stimulated MH-S cells. The suppressive effect of the PBE on phosphorylated (p)-NF- κB translocation was also investigated using IF analysis. This study showed that the PBE suppressed the CFA-induced inflammation in the MH-S cells by suppressing the NF- κB and MAPK signaling pathways, which suggests its potential usefulness in reducing lung inflammation.

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          NF-κB signaling in inflammation

          The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.
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            Pathological roles of MAPK signaling pathways in human diseases.

            The mammalian family of mitogen-activated protein kinases (MAPKs) includes extracellular signal-regulated kinase (ERK), p38, and c-Jun NH(2)-terminal kinase (JNK), with each MAPK signaling pathway consisting of at least three components, a MAPK kinase kinase (MAP3K), a MAPK kinase (MAP2K), and a MAPK. The MAPK pathways are activated by diverse extracellular and intracellular stimuli including peptide growth factors, cytokines, hormones, and various cellular stressors such as oxidative stress and endoplasmic reticulum stress. These signaling pathways regulate a variety of cellular activities including proliferation, differentiation, survival, and death. Deviation from the strict control of MAPK signaling pathways has been implicated in the development of many human diseases including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and various types of cancers. Persistent activation of the JNK or p38 signaling pathways has been suggested to mediate neuronal apoptosis in AD, PD, and ALS, whereas the ERK signaling pathway plays a key role in several steps of tumorigenesis including cancer cell proliferation, migration, and invasion. In this review, we summarize recent findings on the roles of MAPK signaling pathways in human disorders, focusing on cancer and neurodegenerative diseases including AD, PD, and ALS. Copyright 2010 Elsevier B.V. All rights reserved.
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              The impact of PM2.5 on the human respiratory system.

              Recently, many researchers paid more attentions to the association between air pollution and respiratory system disease. In the past few years, levels of smog have increased throughout China resulting in the deterioration of air quality, raising worldwide concerns. PM2.5 (particles less than 2.5 micrometers in diameter) can penetrate deeply into the lung, irritate and corrode the alveolar wall, and consequently impair lung function. Hence it is important to investigate the impact of PM2.5 on the respiratory system and then to help China combat the current air pollution problems. In this review, we will discuss PM2.5 damage on human respiratory system from epidemiological, experimental and mechanism studies. At last, we recommend to the population to limit exposure to air pollution and call to the authorities to create an index of pollution related to health.
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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2021
                25 October 2021
                25 October 2021
                : 2021
                : 5535630
                Affiliations
                1Department of Veterinary Medicine, Cardiovascular Research Institute and College of Veterinary Medicine, Kyungpook National University, Daegu 41566, Republic of Korea
                2Department of Neurobiology, University of Utah, Salt Lake, UT, USA
                3Division of Biotechnology and Advanced Institute of Environment and Bioscience, College of Environmental and Bioresource Sciences, Jeonbuk National University, Gobong-ro 79, Iksan 54596, Republic of Korea
                Author notes

                Academic Editor: Saeideh Saadat

                Author information
                https://orcid.org/0000-0001-6874-3095
                https://orcid.org/0000-0002-5938-3048
                https://orcid.org/0000-0002-0594-8955
                https://orcid.org/0000-0001-9891-8888
                https://orcid.org/0000-0002-3088-1318
                Article
                10.1155/2021/5535630
                8560242
                a2ba2d18-f95f-4da1-bdb2-69fe6abe61bc
                Copyright © 2021 H. M. Arif Ullah et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 June 2021
                : 1 October 2021
                : 11 October 2021
                Funding
                Funded by: National Research Foundation of Korea
                Award ID: 2018R1D1A1A09083797
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

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