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The effect of esculentoside A on lupus nephritis-prone BXSB mice
INTRODUCTION: EsA was reported to have the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects in acute and chronic experimental models. However, the effects of EsA on LN remain poorly understood. To investigate the roles of EsA in LN, the effe...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648817/ https://www.ncbi.nlm.nih.gov/pubmed/23671449 http://dx.doi.org/10.5114/aoms.2012.31439 |
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author | Ma, Hualin Zhang, Xianggui Zhang, Xinzhou Yang, Dan Meng, Lingguo Zhang, Yi Zhou, Shuyan |
author_facet | Ma, Hualin Zhang, Xianggui Zhang, Xinzhou Yang, Dan Meng, Lingguo Zhang, Yi Zhou, Shuyan |
author_sort | Ma, Hualin |
collection | PubMed |
description | INTRODUCTION: EsA was reported to have the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects in acute and chronic experimental models. However, the effects of EsA on LN remain poorly understood. To investigate the roles of EsA in LN, the effects of EsA were tested on BXSB mice, a SLE model, in which male SB/Le mice and female C57BL/6 mice were hybridized through recombinant inbred species. MATERIAL AND METHODS: Twenty four BXSB mice were divided into three groups. After 4 weeks, blood samples, urine samples and kidney tissues were collected. Measurement of cytokine levels was carried out using sandwich ELISA reagent kits. Apoptotic scores were obtained with a TUNEL assay. PCNA and Caspase-3 mRNA was detected using the In Situ Hybridization Detection Kit. RESULTS: The results demonstrated that compared with the control group, EsA administration markedly controlled urine protein excretion, improved renal function, alleviated kidney damage and promoted the apoptosis of glomerular intrinsic cells and renal tubular epithelial cells in animals of the treated group (p < 0.05). Meanwhile, EsA reduced the serum IL-6 and TNF-α levels (p < 0.05), inhibited the expression of PCNA and promoted the expression of caspase-3, Fas and FasL in animals of the treated group (p < 0.05). The effects of EsA on BXSB mice were similar to dexamethasone. CONCLUSIONS: All these findings indicated that EsA might play significant roles in the treatment of BXSB mice through modulation of inflammatory cytokines, inhibition of renal cell proliferation and induction of apoptosis. The special targets of EsA in lupus nephritis are worth further exploration. |
format | Online Article Text |
id | pubmed-3648817 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-36488172013-05-13 The effect of esculentoside A on lupus nephritis-prone BXSB mice Ma, Hualin Zhang, Xianggui Zhang, Xinzhou Yang, Dan Meng, Lingguo Zhang, Yi Zhou, Shuyan Arch Med Sci Experimental Research INTRODUCTION: EsA was reported to have the effect of modulating immune response, cell proliferation and apoptosis as well as anti-inflammatory effects in acute and chronic experimental models. However, the effects of EsA on LN remain poorly understood. To investigate the roles of EsA in LN, the effects of EsA were tested on BXSB mice, a SLE model, in which male SB/Le mice and female C57BL/6 mice were hybridized through recombinant inbred species. MATERIAL AND METHODS: Twenty four BXSB mice were divided into three groups. After 4 weeks, blood samples, urine samples and kidney tissues were collected. Measurement of cytokine levels was carried out using sandwich ELISA reagent kits. Apoptotic scores were obtained with a TUNEL assay. PCNA and Caspase-3 mRNA was detected using the In Situ Hybridization Detection Kit. RESULTS: The results demonstrated that compared with the control group, EsA administration markedly controlled urine protein excretion, improved renal function, alleviated kidney damage and promoted the apoptosis of glomerular intrinsic cells and renal tubular epithelial cells in animals of the treated group (p < 0.05). Meanwhile, EsA reduced the serum IL-6 and TNF-α levels (p < 0.05), inhibited the expression of PCNA and promoted the expression of caspase-3, Fas and FasL in animals of the treated group (p < 0.05). The effects of EsA on BXSB mice were similar to dexamethasone. CONCLUSIONS: All these findings indicated that EsA might play significant roles in the treatment of BXSB mice through modulation of inflammatory cytokines, inhibition of renal cell proliferation and induction of apoptosis. The special targets of EsA in lupus nephritis are worth further exploration. Termedia Publishing House 2012-10-30 2013-04-20 /pmc/articles/PMC3648817/ /pubmed/23671449 http://dx.doi.org/10.5114/aoms.2012.31439 Text en Copyright © 2013 Termedia & Banach http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Experimental Research Ma, Hualin Zhang, Xianggui Zhang, Xinzhou Yang, Dan Meng, Lingguo Zhang, Yi Zhou, Shuyan The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title | The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title_full | The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title_fullStr | The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title_full_unstemmed | The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title_short | The effect of esculentoside A on lupus nephritis-prone BXSB mice |
title_sort | effect of esculentoside a on lupus nephritis-prone bxsb mice |
topic | Experimental Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648817/ https://www.ncbi.nlm.nih.gov/pubmed/23671449 http://dx.doi.org/10.5114/aoms.2012.31439 |
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