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Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9
OBJECTIVE: Acute liver injury (ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride (CCl(4)) is a possible environmental toxicant that can induce ALF. Portulaca oleracea (PO) is one of the most popular edible herbs and has several biological activities such as antioxidant,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975634/ https://www.ncbi.nlm.nih.gov/pubmed/36875440 http://dx.doi.org/10.1016/j.chmed.2022.05.004 |
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author | Qian, Aruna Zhou, Lu Shi, Dongxu Pang, Zongran Lu, Binan |
author_facet | Qian, Aruna Zhou, Lu Shi, Dongxu Pang, Zongran Lu, Binan |
author_sort | Qian, Aruna |
collection | PubMed |
description | OBJECTIVE: Acute liver injury (ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride (CCl(4)) is a possible environmental toxicant that can induce ALF. Portulaca oleracea (PO) is one of the most popular edible herbs and has several biological activities such as antioxidant, antimicrobial, anti-inflammatory effects. We explored the significance of PO in regulating inflammatory function in animal models and cultured hepatocytes during liver damage caused by CCl(4). METHODS: The effect of PO on ALF was evaluated by CCl(4)-induced mice models in vivo. Hepatic levels of transaminase activities and inflammatory factors were examined. The gene and protein expression of S100A8 and S100A9 were measured by RT-PCR and Western blot analysis. Meanwhile, the efficacy of PO was certified by HepG2 cells in vitro. The transaminase activities, inflammatory factors, and the protein expression of S100A8 and S100A9 were also detected. RESULTS: Animal tests showed that pretreatment with PO reduced the liver pathological tissue damage and the serum levels of ALT, AST, ALT and LDH, as well as reducing the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) secretion in CCl(4)-induced liver injury mice. Simultaneously, HepG2 cells pretreated with PO exhibited a significant decrease in the activities of ALT and AST. Moreover, PO resulted in a significant downregulation of the pro-inflammatory markers S100A8, S100A9 gene and protein expression on CCl(4) induced acute liver injury was demonstrated entirely in vivo and vitro experiments. CONCLUSION: PO may down-regulate S100A8 and S100A9 and inhibit pro-inflammatory cytokines' release, indicating a potential clinical effect for controlling the disease. |
format | Online Article Text |
id | pubmed-9975634 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-99756342023-03-02 Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 Qian, Aruna Zhou, Lu Shi, Dongxu Pang, Zongran Lu, Binan Chin Herb Med Original Article OBJECTIVE: Acute liver injury (ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride (CCl(4)) is a possible environmental toxicant that can induce ALF. Portulaca oleracea (PO) is one of the most popular edible herbs and has several biological activities such as antioxidant, antimicrobial, anti-inflammatory effects. We explored the significance of PO in regulating inflammatory function in animal models and cultured hepatocytes during liver damage caused by CCl(4). METHODS: The effect of PO on ALF was evaluated by CCl(4)-induced mice models in vivo. Hepatic levels of transaminase activities and inflammatory factors were examined. The gene and protein expression of S100A8 and S100A9 were measured by RT-PCR and Western blot analysis. Meanwhile, the efficacy of PO was certified by HepG2 cells in vitro. The transaminase activities, inflammatory factors, and the protein expression of S100A8 and S100A9 were also detected. RESULTS: Animal tests showed that pretreatment with PO reduced the liver pathological tissue damage and the serum levels of ALT, AST, ALT and LDH, as well as reducing the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) secretion in CCl(4)-induced liver injury mice. Simultaneously, HepG2 cells pretreated with PO exhibited a significant decrease in the activities of ALT and AST. Moreover, PO resulted in a significant downregulation of the pro-inflammatory markers S100A8, S100A9 gene and protein expression on CCl(4) induced acute liver injury was demonstrated entirely in vivo and vitro experiments. CONCLUSION: PO may down-regulate S100A8 and S100A9 and inhibit pro-inflammatory cytokines' release, indicating a potential clinical effect for controlling the disease. Elsevier 2022-08-13 /pmc/articles/PMC9975634/ /pubmed/36875440 http://dx.doi.org/10.1016/j.chmed.2022.05.004 Text en © 2022 Tianjin Press of Chinese Herbal Medicines. Published by ELSEVIER B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Article Qian, Aruna Zhou, Lu Shi, Dongxu Pang, Zongran Lu, Binan Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title | Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title_full | Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title_fullStr | Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title_full_unstemmed | Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title_short | Portulaca oleracea alleviates CCl(4)-induced acute liver injury by regulating hepatic S100A8 and S100A9 |
title_sort | portulaca oleracea alleviates ccl(4)-induced acute liver injury by regulating hepatic s100a8 and s100a9 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975634/ https://www.ncbi.nlm.nih.gov/pubmed/36875440 http://dx.doi.org/10.1016/j.chmed.2022.05.004 |
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