Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway
ABSTRACT Purpose: To investigate the role of cyanidin-3-O-glucoside (C3G) in renal ischemia/reperfusion (I/R) injury and the potential mechanisms. Methods: Mouse models were established by clamping the left renal vessels, and in vitro cellular models were established by hypoxic reoxygenation. Res...
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| Format: | Article |
| Language: | English |
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Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
2023-05-01
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| Series: | Acta Cirúrgica Brasileira |
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| Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502023000100210&lng=en&tlng=en |
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| author | Yufeng Xiong Jun Jian Honglin Yu Jiejun Wu Hu Mao Ruikang Feng Lei Wang Yonghong Jian Xiuheng Liu |
| author_facet | Yufeng Xiong Jun Jian Honglin Yu Jiejun Wu Hu Mao Ruikang Feng Lei Wang Yonghong Jian Xiuheng Liu |
| author_sort | Yufeng Xiong |
| collection | DOAJ |
| description | ABSTRACT Purpose: To investigate the role of cyanidin-3-O-glucoside (C3G) in renal ischemia/reperfusion (I/R) injury and the potential mechanisms. Methods: Mouse models were established by clamping the left renal vessels, and in vitro cellular models were established by hypoxic reoxygenation. Results: Renal dysfunction and tissue structural damage were significantly higher in the I/R group. After treatment with different concentrations of C3G, the levels of renal dysfunction and tissue structural damage decreased at different levels. And its protective effect was most pronounced at 200 mg/kg. The use of C3G reduced apoptosis as well as the expression of endoplasmic reticulum stress (ERS)-related proteins. Hypoxia/reoxygenation (H/R)-induced apoptosis and ERS are dependent on oxidative stress in vitro. In addition, both AG490 and C3G inhibited the activation of JAK/STAT pathway and attenuated oxidative stress, ischemia-induced apoptosis and ERS. Conclusions: The results demonstrated that C3G blocked renal apoptosis and ERS protein expression by preventing reactive oxygen species (ROS) production after I/R via the JAK/STAT pathway, suggesting that C3G may be a potential therapeutic agent for renal I/R injury. |
| first_indexed | 2024-04-09T14:54:00Z |
| format | Article |
| id | doaj.art-4242d659a81c4c64b55e986ff56a531c |
| institution | Directory Open Access Journal |
| issn | 1678-2674 |
| language | English |
| last_indexed | 2024-04-09T14:54:00Z |
| publishDate | 2023-05-01 |
| publisher | Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia |
| record_format | Article |
| series | Acta Cirúrgica Brasileira |
| spelling | doaj.art-4242d659a81c4c64b55e986ff56a531c2023-05-02T07:32:40ZengSociedade Brasileira para o Desenvolvimento da Pesquisa em CirurgiaActa Cirúrgica Brasileira1678-26742023-05-013810.1590/acb381023Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathwayYufeng Xionghttps://orcid.org/0000-0001-9810-1691Jun Jianhttps://orcid.org/0000-0002-1406-4668Honglin Yuhttps://orcid.org/0000-0001-5330-2182Jiejun Wuhttps://orcid.org/0009-0008-6094-1423Hu Maohttps://orcid.org/0000-0003-2252-5572Ruikang Fenghttps://orcid.org/0000-0002-3228-3434Lei Wanghttps://orcid.org/0000-0001-8412-1130Yonghong Jianhttps://orcid.org/0000-0002-9719-2103Xiuheng Liuhttps://orcid.org/0000-0003-3882-2715ABSTRACT Purpose: To investigate the role of cyanidin-3-O-glucoside (C3G) in renal ischemia/reperfusion (I/R) injury and the potential mechanisms. Methods: Mouse models were established by clamping the left renal vessels, and in vitro cellular models were established by hypoxic reoxygenation. Results: Renal dysfunction and tissue structural damage were significantly higher in the I/R group. After treatment with different concentrations of C3G, the levels of renal dysfunction and tissue structural damage decreased at different levels. And its protective effect was most pronounced at 200 mg/kg. The use of C3G reduced apoptosis as well as the expression of endoplasmic reticulum stress (ERS)-related proteins. Hypoxia/reoxygenation (H/R)-induced apoptosis and ERS are dependent on oxidative stress in vitro. In addition, both AG490 and C3G inhibited the activation of JAK/STAT pathway and attenuated oxidative stress, ischemia-induced apoptosis and ERS. Conclusions: The results demonstrated that C3G blocked renal apoptosis and ERS protein expression by preventing reactive oxygen species (ROS) production after I/R via the JAK/STAT pathway, suggesting that C3G may be a potential therapeutic agent for renal I/R injury.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502023000100210&lng=en&tlng=enOxidative StressApoptosisIschemiaReperfusionApoptosis, Endoplasmic Reticulum Stress |
| spellingShingle | Yufeng Xiong Jun Jian Honglin Yu Jiejun Wu Hu Mao Ruikang Feng Lei Wang Yonghong Jian Xiuheng Liu Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway Acta Cirúrgica Brasileira Oxidative Stress Apoptosis Ischemia Reperfusion Apoptosis, Endoplasmic Reticulum Stress |
| title | Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway |
| title_full | Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway |
| title_fullStr | Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway |
| title_full_unstemmed | Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway |
| title_short | Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway |
| title_sort | cyanidin 3 o glucoside plays a protective role against renal ischemia reperfusion injury via the jak stat pathway |
| topic | Oxidative Stress Apoptosis Ischemia Reperfusion Apoptosis, Endoplasmic Reticulum Stress |
| url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502023000100210&lng=en&tlng=en |
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