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Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice
Systemic lupus erythaematosus (SLE) is a chronic multi-system autoimmune disease with a high prevalence of kidney and cardiovascular complications. Considering that Rho-associated coiled-coil-containing protein kinases (ROCKs) play important roles in SLE, inflammation, and cardiovascular disease, we...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316987/ https://www.ncbi.nlm.nih.gov/pubmed/32636749 http://dx.doi.org/10.3389/fphar.2020.00929 |
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author | Yan, Yu Zhang, Zhihui Chen, Yucai Hou, Biyu Liu, Kang Qin, Hailin Fang, Lianhua Du, Guanhua |
author_facet | Yan, Yu Zhang, Zhihui Chen, Yucai Hou, Biyu Liu, Kang Qin, Hailin Fang, Lianhua Du, Guanhua |
author_sort | Yan, Yu |
collection | PubMed |
description | Systemic lupus erythaematosus (SLE) is a chronic multi-system autoimmune disease with a high prevalence of kidney and cardiovascular complications. Considering that Rho-associated coiled-coil-containing protein kinases (ROCKs) play important roles in SLE, inflammation, and cardiovascular disease, we hypothesized that coptisine, which has been found to inhibit ROCKs, may have an effect on SLE. The effect of coptisine was assessed in female BALB/c mice intraperitoneally injected with 0.5 mL of pristane. Serum autoantibodies were tested every month, blood pressure was measured every 2 months, and serum inflammatory markers, spleen pathologic characteristics, renal injury and vascular function were observed at 6 months. The results showed that coptisine decreased the levels of serum autoantibodies and serum inflammatory markers in the SLE mice, improved the pathologic characteristics of the spleen, and simultaneously improved renal injury, decreased inflammatory responses in the kidneys, reduced blood pressure, and improved vascular endothelial function. Western blot assays revealed that inhibiting the activation of the NF-κB and Rho/ROCK signalling pathways and downstream signalling molecules might be the potential mechanisms of the effects of coptisine. Our findings suggest that therapy with coptisine may be a strategy for preventing SLE and ameliorating associated kidney and cardiovascular complications. |
format | Online Article Text |
id | pubmed-7316987 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73169872020-07-06 Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice Yan, Yu Zhang, Zhihui Chen, Yucai Hou, Biyu Liu, Kang Qin, Hailin Fang, Lianhua Du, Guanhua Front Pharmacol Pharmacology Systemic lupus erythaematosus (SLE) is a chronic multi-system autoimmune disease with a high prevalence of kidney and cardiovascular complications. Considering that Rho-associated coiled-coil-containing protein kinases (ROCKs) play important roles in SLE, inflammation, and cardiovascular disease, we hypothesized that coptisine, which has been found to inhibit ROCKs, may have an effect on SLE. The effect of coptisine was assessed in female BALB/c mice intraperitoneally injected with 0.5 mL of pristane. Serum autoantibodies were tested every month, blood pressure was measured every 2 months, and serum inflammatory markers, spleen pathologic characteristics, renal injury and vascular function were observed at 6 months. The results showed that coptisine decreased the levels of serum autoantibodies and serum inflammatory markers in the SLE mice, improved the pathologic characteristics of the spleen, and simultaneously improved renal injury, decreased inflammatory responses in the kidneys, reduced blood pressure, and improved vascular endothelial function. Western blot assays revealed that inhibiting the activation of the NF-κB and Rho/ROCK signalling pathways and downstream signalling molecules might be the potential mechanisms of the effects of coptisine. Our findings suggest that therapy with coptisine may be a strategy for preventing SLE and ameliorating associated kidney and cardiovascular complications. Frontiers Media S.A. 2020-06-19 /pmc/articles/PMC7316987/ /pubmed/32636749 http://dx.doi.org/10.3389/fphar.2020.00929 Text en Copyright © 2020 Yan, Zhang, Chen, Hou, Liu, Qin, Fang and Du http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Pharmacology Yan, Yu Zhang, Zhihui Chen, Yucai Hou, Biyu Liu, Kang Qin, Hailin Fang, Lianhua Du, Guanhua Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title | Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title_full | Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title_fullStr | Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title_full_unstemmed | Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title_short | Coptisine Alleviates Pristane-Induced Lupus-Like Disease and Associated Kidney and Cardiovascular Complications in Mice |
title_sort | coptisine alleviates pristane-induced lupus-like disease and associated kidney and cardiovascular complications in mice |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7316987/ https://www.ncbi.nlm.nih.gov/pubmed/32636749 http://dx.doi.org/10.3389/fphar.2020.00929 |
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