Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis
Introduction: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus. As murine models of LN are valuable tools to better understand its pathophysiology and to search for new effective treatments, we investigated the effects of the bioflavonoid quercetin on pris...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2018-02-01
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| Series: | Autoimmunity |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/08916934.2018.1442828 |
| _version_ | 1827817511492517888 |
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| author | Mariane dos Santos Priscila Tamar Poletti Gaia Favero Alessandra Stacchiotti Francesca Bonomini Carolina Caruccio Montanari Silvia Regina Bona Norma Possa Marroni Rita Rezzani Francisco Veríssimo Veronese |
| author_facet | Mariane dos Santos Priscila Tamar Poletti Gaia Favero Alessandra Stacchiotti Francesca Bonomini Carolina Caruccio Montanari Silvia Regina Bona Norma Possa Marroni Rita Rezzani Francisco Veríssimo Veronese |
| author_sort | Mariane dos Santos |
| collection | DOAJ |
| description | Introduction: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus. As murine models of LN are valuable tools to better understand its pathophysiology and to search for new effective treatments, we investigated the effects of the bioflavonoid quercetin on pristane-induced LN mice through histomorphological analyses. Methods: Immunofluorescence and biochemical assays were used to evaluate the expression of markers of inflammation (interleukin-6, IL-6; tumour necrosis factor-α, TNF-α), oxidative stress (catalase, CAT; superoxide dismutase 1, SOD1; thiobarbituric acid reactive substances, TBARS), apoptosis (Bax), and fibrosis (transforming growth factor-β1, TGF-β1). Glomerular and tubular ultrastructure was analysed, and tissue messenger RNA of podocin, podoplanin and α3β1-integrin were quantified using the real-time polymerase chain reaction. Results: Pristane-induced LN mice showed severe kidney injury, characterized by increased proteinuria, glomerular mesangial expansion and inflammation, high expression of the pro-fibrotic, apoptotic and prooxidant markers and reduction of antioxidants. In the kidney ultrastructure, foot process (FP) effacement, apoptotic mesangial cells and abnormal mitochondria with disrupted cristae were observed, along with suppressed tissue mRNA of podocin, podoplanin and α3β1-integrin. Treatment with quercetin in the pristane-induced LN mice model was nephroprotective, decreasing proteinuria levels and significantly lowering tissue expression of IL-6, TNF-α, TGF-β1, Bax and TBARS. Simultaneously, quercetin significantly increased CAT and SOD1 expressions in these mice. In addition, it was observed improvement of the kidney ultrastructure, and tissue mRNA of podocin, but not podoplanin and α3β1-integrin, was restored to the levels found in the control mice. Conclusion: In conclusion, these findings provide experimental evidence of the renoprotective effects of quercetin in the pristane-induced LN mice model. We suggest that quercetin effectively ameliorates the kidney damage caused by pristane, a bioflavonoid to be further evaluated as a new therapeutic strategy in this disease. |
| first_indexed | 2024-03-12T00:35:12Z |
| format | Article |
| id | doaj.art-7aff048da3844f2a8ae88275ee3aa041 |
| institution | Directory Open Access Journal |
| issn | 0891-6934 1607-842X |
| language | English |
| last_indexed | 2024-03-12T00:35:12Z |
| publishDate | 2018-02-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Autoimmunity |
| spelling | doaj.art-7aff048da3844f2a8ae88275ee3aa0412023-09-15T10:01:07ZengTaylor & Francis GroupAutoimmunity0891-69341607-842X2018-02-01512698010.1080/08916934.2018.14428281442828Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritisMariane dos Santos0Priscila Tamar Poletti1Gaia Favero2Alessandra Stacchiotti3Francesca Bonomini4Carolina Caruccio Montanari5Silvia Regina Bona6Norma Possa Marroni7Rita Rezzani8Francisco Veríssimo Veronese9Universidade Federal do Rio Grande do SulUniversidade Federal do Rio Grande do SulUniversity of BresciaUniversity of BresciaUniversity of BresciaUniversidade Federal do Rio Grande do SulHospital de Clínicas de Porto AlegreHospital de Clínicas de Porto AlegreUniversity of BresciaUniversidade Federal do Rio Grande do SulIntroduction: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus. As murine models of LN are valuable tools to better understand its pathophysiology and to search for new effective treatments, we investigated the effects of the bioflavonoid quercetin on pristane-induced LN mice through histomorphological analyses. Methods: Immunofluorescence and biochemical assays were used to evaluate the expression of markers of inflammation (interleukin-6, IL-6; tumour necrosis factor-α, TNF-α), oxidative stress (catalase, CAT; superoxide dismutase 1, SOD1; thiobarbituric acid reactive substances, TBARS), apoptosis (Bax), and fibrosis (transforming growth factor-β1, TGF-β1). Glomerular and tubular ultrastructure was analysed, and tissue messenger RNA of podocin, podoplanin and α3β1-integrin were quantified using the real-time polymerase chain reaction. Results: Pristane-induced LN mice showed severe kidney injury, characterized by increased proteinuria, glomerular mesangial expansion and inflammation, high expression of the pro-fibrotic, apoptotic and prooxidant markers and reduction of antioxidants. In the kidney ultrastructure, foot process (FP) effacement, apoptotic mesangial cells and abnormal mitochondria with disrupted cristae were observed, along with suppressed tissue mRNA of podocin, podoplanin and α3β1-integrin. Treatment with quercetin in the pristane-induced LN mice model was nephroprotective, decreasing proteinuria levels and significantly lowering tissue expression of IL-6, TNF-α, TGF-β1, Bax and TBARS. Simultaneously, quercetin significantly increased CAT and SOD1 expressions in these mice. In addition, it was observed improvement of the kidney ultrastructure, and tissue mRNA of podocin, but not podoplanin and α3β1-integrin, was restored to the levels found in the control mice. Conclusion: In conclusion, these findings provide experimental evidence of the renoprotective effects of quercetin in the pristane-induced LN mice model. We suggest that quercetin effectively ameliorates the kidney damage caused by pristane, a bioflavonoid to be further evaluated as a new therapeutic strategy in this disease.http://dx.doi.org/10.1080/08916934.2018.1442828lupus nephritispristanequercetininflammationoxidative stresspodocyte |
| spellingShingle | Mariane dos Santos Priscila Tamar Poletti Gaia Favero Alessandra Stacchiotti Francesca Bonomini Carolina Caruccio Montanari Silvia Regina Bona Norma Possa Marroni Rita Rezzani Francisco Veríssimo Veronese Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis Autoimmunity lupus nephritis pristane quercetin inflammation oxidative stress podocyte |
| title | Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis |
| title_full | Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis |
| title_fullStr | Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis |
| title_full_unstemmed | Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis |
| title_short | Protective effects of quercetin treatment in a pristane-induced mouse model of lupus nephritis |
| title_sort | protective effects of quercetin treatment in a pristane induced mouse model of lupus nephritis |
| topic | lupus nephritis pristane quercetin inflammation oxidative stress podocyte |
| url | http://dx.doi.org/10.1080/08916934.2018.1442828 |
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