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Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors
The study aimed to investigate the role of Tanshinone IIA (Tan IIA) in lipopolysaccharide (LPS)‐induced acute lung injury (ALI) in its regulation of TRPM7. Wistar male rats were randomly divided into the normal saline (NS), LPS, knockout (KO) + LPS, low‐dose Tan IIA (Tan‐L), middle‐dose Tan IIA (Tan...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5742685/ https://www.ncbi.nlm.nih.gov/pubmed/29047214 http://dx.doi.org/10.1111/jcmm.13350 |
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author | Li, Jie Zheng, Yan Li, Ming‐Xian Yang, Chu‐Wei Liu, Yu‐Fei |
author_facet | Li, Jie Zheng, Yan Li, Ming‐Xian Yang, Chu‐Wei Liu, Yu‐Fei |
author_sort | Li, Jie |
collection | PubMed |
description | The study aimed to investigate the role of Tanshinone IIA (Tan IIA) in lipopolysaccharide (LPS)‐induced acute lung injury (ALI) in its regulation of TRPM7. Wistar male rats were randomly divided into the normal saline (NS), LPS, knockout (KO) + LPS, low‐dose Tan IIA (Tan‐L), middle‐dose Tan IIA (Tan‐M), high‐dose Tan IIA (Tan‐H) and KO + high‐dose Tan IIA (KO + Tan‐H) groups. The level of tumour necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, TRPM7 protein expression, current density‐voltage curve and Ca(2+) concentration were detected through ELISA, Western blotting, electrophysiological experiment and a calcium‐imaging technique, respectively. The rats in the KO + LPS, Tan‐L, Tan‐M, Tan‐H and KO + Tan‐H groups all displayed lower levels of TNF‐α, IL‐1β and IL‐6 than the LPS group. Rats in the KO + Tan‐H group exhibited lower levels of NF‐α, IL‐1β and IL‐6 than rats in the Tan‐H group. Elevated levels of TRPM7 protein expression in the LPS and Tan groups were detected in comparison with the NS group. However, TRPM7 protein expression in Tan‐M and Tan‐H groups was notably lower than in that of the LPS group. In comparison with the NS group, the LPS and Tan groups had a greater PIMs cell density and a higher concentration of Ca(2+). Contrary results were observed in the KO + LPS, Tan‐H and KO + Tan‐H groups. Tan IIA decreases calcium influx in PIMs and inhibits pro‐inflammatory factors which provide an alleviatory effect in regards to LPS‐induced ALI by suppressing TRPM7 expression. |
format | Online Article Text |
id | pubmed-5742685 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57426852018-01-04 Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors Li, Jie Zheng, Yan Li, Ming‐Xian Yang, Chu‐Wei Liu, Yu‐Fei J Cell Mol Med Original Articles The study aimed to investigate the role of Tanshinone IIA (Tan IIA) in lipopolysaccharide (LPS)‐induced acute lung injury (ALI) in its regulation of TRPM7. Wistar male rats were randomly divided into the normal saline (NS), LPS, knockout (KO) + LPS, low‐dose Tan IIA (Tan‐L), middle‐dose Tan IIA (Tan‐M), high‐dose Tan IIA (Tan‐H) and KO + high‐dose Tan IIA (KO + Tan‐H) groups. The level of tumour necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, TRPM7 protein expression, current density‐voltage curve and Ca(2+) concentration were detected through ELISA, Western blotting, electrophysiological experiment and a calcium‐imaging technique, respectively. The rats in the KO + LPS, Tan‐L, Tan‐M, Tan‐H and KO + Tan‐H groups all displayed lower levels of TNF‐α, IL‐1β and IL‐6 than the LPS group. Rats in the KO + Tan‐H group exhibited lower levels of NF‐α, IL‐1β and IL‐6 than rats in the Tan‐H group. Elevated levels of TRPM7 protein expression in the LPS and Tan groups were detected in comparison with the NS group. However, TRPM7 protein expression in Tan‐M and Tan‐H groups was notably lower than in that of the LPS group. In comparison with the NS group, the LPS and Tan groups had a greater PIMs cell density and a higher concentration of Ca(2+). Contrary results were observed in the KO + LPS, Tan‐H and KO + Tan‐H groups. Tan IIA decreases calcium influx in PIMs and inhibits pro‐inflammatory factors which provide an alleviatory effect in regards to LPS‐induced ALI by suppressing TRPM7 expression. John Wiley and Sons Inc. 2017-10-18 2018-01 /pmc/articles/PMC5742685/ /pubmed/29047214 http://dx.doi.org/10.1111/jcmm.13350 Text en © 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Li, Jie Zheng, Yan Li, Ming‐Xian Yang, Chu‐Wei Liu, Yu‐Fei Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title | Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title_full | Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title_fullStr | Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title_full_unstemmed | Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title_short | Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors |
title_sort | tanshinone iia alleviates lipopolysaccharide‐induced acute lung injury by downregulating trpm7 and pro‐inflammatory factors |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5742685/ https://www.ncbi.nlm.nih.gov/pubmed/29047214 http://dx.doi.org/10.1111/jcmm.13350 |
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