Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling
Abstract Background Acute myocardial infarction (AMI) is the leading cause of death globally and has thus placed a heavy burden on healthcare. Tanshinone IIA (TSA) is a major active compound, extracted from Salvia miltiorrhiza Bunge, that possesses various pharmacological activities. The aim of the...
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| Format: | Article |
| Language: | English |
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BMC
2020-03-01
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| Series: | BMC Molecular and Cell Biology |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s12860-020-00264-3 |
| _version_ | 1819022929186258944 |
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| author | Liye Chen Lili Wei Qiongyang Yu Haozhe Shi George Liu |
| author_facet | Liye Chen Lili Wei Qiongyang Yu Haozhe Shi George Liu |
| author_sort | Liye Chen |
| collection | DOAJ |
| description | Abstract Background Acute myocardial infarction (AMI) is the leading cause of death globally and has thus placed a heavy burden on healthcare. Tanshinone IIA (TSA) is a major active compound, extracted from Salvia miltiorrhiza Bunge, that possesses various pharmacological activities. The aim of the present study was to investigate the role of TSA in AMI and its underlying mechanism of action. Results: We have shown that TSA decreased the apoptosis rate, the amount of LDH, MDA as well as ROS of cardiomyocytes. Meantime, it elevated mitochondrial membrane potential (MMP) which was decreased by H/R treatment. It was also determined that miR-124-5p targets AK003290 directly. TSA up-regulated the expression of AK003290 and its function can be reversed by knock down of AK003290 as well as miR-124-5p overexpression. Conclusion TSA exerts the protective role against H/R induced apoptosis, oxidative and MMP loss of cardiomyocytes via regulating AK003290 and miR-124-5p signaling. |
| first_indexed | 2024-12-21T04:30:48Z |
| format | Article |
| id | doaj.art-25cc5a4ebdfe4cbfa696b1bba03dba17 |
| institution | Directory Open Access Journal |
| issn | 2661-8850 |
| language | English |
| last_indexed | 2024-12-21T04:30:48Z |
| publishDate | 2020-03-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Molecular and Cell Biology |
| spelling | doaj.art-25cc5a4ebdfe4cbfa696b1bba03dba172022-12-21T19:15:56ZengBMCBMC Molecular and Cell Biology2661-88502020-03-0121111010.1186/s12860-020-00264-3Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signalingLiye Chen0Lili Wei1Qiongyang Yu2Haozhe Shi3George Liu4Key Laboratory of Molecular Cardiovascular Science Ministry of Education; Institute of Cardiovascular Sciences, Health Science Center, Peking UniversitySchool of Medicine, Shihezi UniversityKey Laboratory of Molecular Cardiovascular Science Ministry of Education; Institute of Cardiovascular Sciences, Health Science Center, Peking UniversityKey Laboratory of Molecular Cardiovascular Science Ministry of Education; Institute of Cardiovascular Sciences, Health Science Center, Peking UniversityKey Laboratory of Molecular Cardiovascular Science Ministry of Education; Institute of Cardiovascular Sciences, Health Science Center, Peking UniversityAbstract Background Acute myocardial infarction (AMI) is the leading cause of death globally and has thus placed a heavy burden on healthcare. Tanshinone IIA (TSA) is a major active compound, extracted from Salvia miltiorrhiza Bunge, that possesses various pharmacological activities. The aim of the present study was to investigate the role of TSA in AMI and its underlying mechanism of action. Results: We have shown that TSA decreased the apoptosis rate, the amount of LDH, MDA as well as ROS of cardiomyocytes. Meantime, it elevated mitochondrial membrane potential (MMP) which was decreased by H/R treatment. It was also determined that miR-124-5p targets AK003290 directly. TSA up-regulated the expression of AK003290 and its function can be reversed by knock down of AK003290 as well as miR-124-5p overexpression. Conclusion TSA exerts the protective role against H/R induced apoptosis, oxidative and MMP loss of cardiomyocytes via regulating AK003290 and miR-124-5p signaling.http://link.springer.com/article/10.1186/s12860-020-00264-3Tanshinone IIAAcute myocardial infarctionmiR-124-5pAK003290 |
| spellingShingle | Liye Chen Lili Wei Qiongyang Yu Haozhe Shi George Liu Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling BMC Molecular and Cell Biology Tanshinone IIA Acute myocardial infarction miR-124-5p AK003290 |
| title | Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling |
| title_full | Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling |
| title_fullStr | Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling |
| title_full_unstemmed | Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling |
| title_short | Tanshinone IIA alleviates hypoxia/reoxygenation induced cardiomyocyte injury via lncRNA AK003290/miR-124-5p signaling |
| title_sort | tanshinone iia alleviates hypoxia reoxygenation induced cardiomyocyte injury via lncrna ak003290 mir 124 5p signaling |
| topic | Tanshinone IIA Acute myocardial infarction miR-124-5p AK003290 |
| url | http://link.springer.com/article/10.1186/s12860-020-00264-3 |
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