Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis
Sunitinib (SU), a multi-targeted tyrosine kinase inhibitor, has anticancer function but its clinical use is often limited by cardiovascular complications. Baicalin (BA) has demonstrated various pharmacological activities including antioxidant, anti-inflammatory and antiviral properties, but its pote...
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Frontiers Media S.A.
2025-04-01
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2025.1563194/full |
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| author | Zefu Yang Zefu Yang Jianping Wan Xinjin Zhang Jiaqi Mei Hua Hao Sibo Liu Yun Yi Meixiu Jiang Yuanqiao He Yuanqiao He Yuanqiao He |
| author_facet | Zefu Yang Zefu Yang Jianping Wan Xinjin Zhang Jiaqi Mei Hua Hao Sibo Liu Yun Yi Meixiu Jiang Yuanqiao He Yuanqiao He Yuanqiao He |
| author_sort | Zefu Yang |
| collection | DOAJ |
| description | Sunitinib (SU), a multi-targeted tyrosine kinase inhibitor, has anticancer function but its clinical use is often limited by cardiovascular complications. Baicalin (BA) has demonstrated various pharmacological activities including antioxidant, anti-inflammatory and antiviral properties, but its potential roles in SU-induced cardiotoxicity have not been reported. In this study, we aimed to investigate the effect of BA in SU-induced cardiotoxicity in vivo by using renal carcinoma patient-derived xenograft (PDX) model. Female Nod Scid mice with renal carcinoma PDX were treated with vehicle, SU (50 mg/kg/d), BA (100 mg/kg/d), or BA combined with SU for 6 weeks. The tumor volume and weight of tumor-bearing mice were measured, and cardiovascular functions were evaluated by testing the Heart index and blood biochemical indicators, and by hematoxylin and eosin (H&E), Masson and Tunel staining. The results showed that SU therapy and combination therapy effectively inhibited the growth of renal tumors. Combination therapy inhibited SU-induced increase of creatine kinase (CK) and lactate dehydrogenase (LDH), and ameliorated the heart parameters. Moreover, BA effectively protected SU-induced cardiac dysfunction by decreasing injury, apoptosis, and fibrosis. Collectively, our results demonstrate that BA can be as a potential cardioprotective approach for cardiovascular complications during SU regimen. |
| format | Article |
| id | doaj-art-5faadaad237540c4b455bf4bd076e504 |
| institution | OA Journals |
| issn | 1663-9812 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pharmacology |
| spelling | doaj-art-5faadaad237540c4b455bf4bd076e5042025-08-20T02:08:26ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-04-011610.3389/fphar.2025.15631941563194Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosisZefu Yang0Zefu Yang1Jianping Wan2Xinjin Zhang3Jiaqi Mei4Hua Hao5Sibo Liu6Yun Yi7Meixiu Jiang8Yuanqiao He9Yuanqiao He10Yuanqiao He11Cardiovascular Medicine Department of Nanhai District People’s Hospital, Foshan, Guangdong, ChinaCardiovascular Medicine Department of The Sixth Affiliated Hospital, School of Medicine, South China University of Technology, Foshan, ChinaElectrophysiology Department of The Sixth Affiliated Hospital, School of Medicine, South China University of Technology, Foshan, ChinaCardiovascular Center, Affiliated Hospital of Yunnan University, Kunming, ChinaDepartment of Hematology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, ChinaDepartment of Pathology, Yangpu District Central Hospital, School of Medicine, Tongji University, Shanghai, ChinaThe Queen MARY school, Jiangxi Medical College, Nanchang University, Nanchang, ChinaCenter of Biobank, Nanchang University Second Affiliated Hospital, Jiangxi Medical College, Nanchang, ChinaThe Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, China0Center of Laboratory Animal Science, Nanchang University, Nanchang, China1Jiangxi Province Key Laboratory of Laboratory Animal, Nanchang, China2Nanchang Royo Biotechnology, Nanchang, ChinaSunitinib (SU), a multi-targeted tyrosine kinase inhibitor, has anticancer function but its clinical use is often limited by cardiovascular complications. Baicalin (BA) has demonstrated various pharmacological activities including antioxidant, anti-inflammatory and antiviral properties, but its potential roles in SU-induced cardiotoxicity have not been reported. In this study, we aimed to investigate the effect of BA in SU-induced cardiotoxicity in vivo by using renal carcinoma patient-derived xenograft (PDX) model. Female Nod Scid mice with renal carcinoma PDX were treated with vehicle, SU (50 mg/kg/d), BA (100 mg/kg/d), or BA combined with SU for 6 weeks. The tumor volume and weight of tumor-bearing mice were measured, and cardiovascular functions were evaluated by testing the Heart index and blood biochemical indicators, and by hematoxylin and eosin (H&E), Masson and Tunel staining. The results showed that SU therapy and combination therapy effectively inhibited the growth of renal tumors. Combination therapy inhibited SU-induced increase of creatine kinase (CK) and lactate dehydrogenase (LDH), and ameliorated the heart parameters. Moreover, BA effectively protected SU-induced cardiac dysfunction by decreasing injury, apoptosis, and fibrosis. Collectively, our results demonstrate that BA can be as a potential cardioprotective approach for cardiovascular complications during SU regimen.https://www.frontiersin.org/articles/10.3389/fphar.2025.1563194/fullbaicalinsunitinibcardiotoxicityrenal carcinomaPDX |
| spellingShingle | Zefu Yang Zefu Yang Jianping Wan Xinjin Zhang Jiaqi Mei Hua Hao Sibo Liu Yun Yi Meixiu Jiang Yuanqiao He Yuanqiao He Yuanqiao He Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis Frontiers in Pharmacology baicalin sunitinib cardiotoxicity renal carcinoma PDX |
| title | Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis |
| title_full | Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis |
| title_fullStr | Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis |
| title_full_unstemmed | Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis |
| title_short | Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis |
| title_sort | baicalin reduces sunitinib induced cardiotoxicity in renal carcinoma pdx model by inhibiting myocardial injury apoptosis and fibrosis |
| topic | baicalin sunitinib cardiotoxicity renal carcinoma PDX |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2025.1563194/full |
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