In vivo and in vitro protective effects of shengmai injection against doxorubicin-induced cardiotoxicity
Shengmai injection (SMI) has been used to treat heart failure. This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX). In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H...
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| Published in | Pharmaceutical biology Vol. 60; no. 1; pp. 638 - 651 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Taylor & Francis
31.12.2022
Taylor & Francis Ltd Taylor & Francis Group |
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| Online Access | Get full text |
| ISSN | 1388-0209 1744-5116 1744-5116 |
| DOI | 10.1080/13880209.2022.2046801 |
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| Abstract | Shengmai injection (SMI) has been used to treat heart failure.
This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX).
In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed.
SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway.
This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. |
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| AbstractList | Shengmai injection (SMI) has been used to treat heart failure.CONTEXTShengmai injection (SMI) has been used to treat heart failure.This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX).OBJECTIVEThis study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX).In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed.MATERIALS AND METHODSIn vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed.SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway.RESULTSSMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway.This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway.CONCLUSIONSThis study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. Shengmai injection (SMI) has been used to treat heart failure. This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX). In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed. SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway. This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. Shengmai injection (SMI) has been used to treat heart failure. This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX). , DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. , H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed. SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group . Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway. This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. ContextShengmai injection (SMI) has been used to treat heart failure.ObjectiveThis study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX).Materials and methodsIn vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed.ResultsSMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway.ConclusionsThis study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. Shengmai injection (SMI) has been used to treat heart failure. This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX). In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed. SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway. This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. Context Shengmai injection (SMI) has been used to treat heart failure.Objective This study determines the molecular mechanisms of SMI against cardiotoxicity caused by doxorubicin (DOX).Materials and methods In vivo, DOX (15 mg/kg) was intraperitoneally injected in model, Dex (dexrazoxane), SMI-L (2.7 mL/kg), SMI-M (5.4 mL/kg), and SMI-H (10.8 mL/kg) for 7 consecutive days. Hematoxylin-eosin (HE) and Masson staining were used to evaluate histological changes, and cardiomyocyte apoptosis was identified using TdT-mediated dUTP nick-end labelling (TUNEL). Enzymatic indexes were determined. mRNA and protein expressions were analysed through RT-qPCR and Western blotting. In vitro, H9c2 cells were divided into control group, model group (2 mL 1 μM DOX), SMI group, ML385 group, and SMI + ML385 group, the intervention lasted for 24 h. mRNA and protein expressions were analysed.Results SMI markedly improved cardiac pathology, decreased cardiomyocyte apoptosis, increased creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), decreased superoxide dismutase (SOD). Compared with the model group, the protein expression of nuclear factor erythroid2-related factor 2 (Nrf2) (SMI-L: 2.42-fold, SMI-M: 2.67-fold, SMI-H: 3.07-fold) and haem oxygenase-1(HO-1) (SMI-L: 1.64-fold, SMI-M: 2.01-fold, SMI-H: 2.19-fold) was increased and the protein expression of kelch-like ECH-associated protein 1 (Keap1) (SMI-L: 0.90-fold, SMI-M: 0.77-fold, SMI-H: 0.66-fold) was decreased in SMI groups and Dex group in vivo. Additionally, SMI dramatically inhibited apoptosis, decreased CK, LDH and MDA levels, and enhanced SOD activity. Our results demonstrated that SMI reduced DOX-induced cardiotoxicity via activation of the Nrf2/Keap1 signalling pathway.Conclusions This study revealed a new mechanism by which SMI alleviates DOX-induced 45 cardiomyopathy by modulating the Nrf2/Keap1 signal pathway. |
| Author | Song, Rui Gao, Ge Shi, Hui Li, Jing-ya Wang, Shu-shu Wang, Liang Zhao, Chun-chun Peng, Jian-fei Zhou, Peng |
| Author_xml | – sequence: 1 givenname: Peng surname: Zhou fullname: Zhou, Peng organization: Anhui Province Key Laboratory of Chinese Medicinal Formula – sequence: 2 givenname: Ge surname: Gao fullname: Gao, Ge organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 3 givenname: Chun-chun surname: Zhao fullname: Zhao, Chun-chun organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 4 givenname: Jing-ya surname: Li fullname: Li, Jing-ya organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 5 givenname: Jian-fei surname: Peng fullname: Peng, Jian-fei organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 6 givenname: Shu-shu surname: Wang fullname: Wang, Shu-shu organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 7 givenname: Rui surname: Song fullname: Song, Rui organization: School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine – sequence: 8 givenname: Hui surname: Shi fullname: Shi, Hui organization: Nursing School, Anhui University of Chinese Medicine – sequence: 9 givenname: Liang surname: Wang fullname: Wang, Liang organization: Anhui Province Key Laboratory of Chinese Medicinal Formula |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35298357$$D View this record in MEDLINE/PubMed |
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| Keywords | oxidative apoptosis DOX Nrf2/Keap1 signal pathway |
| Language | English |
| License | open-access: http://creativecommons.org/licenses/by/4.0/: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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| References | e_1_3_4_4_1 e_1_3_4_3_1 e_1_3_4_2_1 e_1_3_4_9_1 e_1_3_4_8_1 e_1_3_4_7_1 e_1_3_4_20_1 e_1_3_4_40_1 e_1_3_4_5_1 e_1_3_4_23_1 e_1_3_4_24_1 e_1_3_4_21_1 e_1_3_4_22_1 e_1_3_4_27_1 e_1_3_4_28_1 e_1_3_4_25_1 Wang Y (e_1_3_4_35_1) 2020; 2020 e_1_3_4_26_1 e_1_3_4_29_1 e_1_3_4_31_1 e_1_3_4_30_1 e_1_3_4_12_1 Chen Y (e_1_3_4_6_1) 2015; 2015 e_1_3_4_13_1 e_1_3_4_34_1 e_1_3_4_10_1 e_1_3_4_33_1 e_1_3_4_11_1 e_1_3_4_32_1 e_1_3_4_16_1 e_1_3_4_39_1 e_1_3_4_17_1 e_1_3_4_38_1 e_1_3_4_14_1 e_1_3_4_37_1 e_1_3_4_15_1 e_1_3_4_36_1 e_1_3_4_18_1 e_1_3_4_19_1 |
| References_xml | – ident: e_1_3_4_5_1 doi: 10.1016/j.toxlet.2017.04.010 – ident: e_1_3_4_28_1 doi: 10.1089/ars.2020.8016 – ident: e_1_3_4_34_1 doi: 10.1016/j.abb.2021.109050 – volume: 2020 start-page: 9571627 year: 2020 ident: e_1_3_4_35_1 article-title: Efficacy and safety of shengmai injection for chronic heart failure: a systematic review of randomized controlled trials publication-title: Evid Based Complement Alternat Med doi: 10.1155/2020/9571627 – ident: e_1_3_4_21_1 doi: 10.1016/j.biopha.2018.04.180 – ident: e_1_3_4_3_1 doi: 10.1007/s00011-019-01292-2 – ident: e_1_3_4_14_1 doi: 10.1080/13880209.2020.1845747 – ident: e_1_3_4_16_1 doi: 10.1002/cmdc.201300525 – ident: e_1_3_4_26_1 doi: 10.1016/j.biopha.2021.111708 – ident: e_1_3_4_40_1 doi: 10.1016/j.jep.2019.01.001 – ident: e_1_3_4_24_1 doi: 10.1155/2021/8898919 – ident: e_1_3_4_22_1 doi: 10.1080/13880209.2021.2007269 – ident: e_1_3_4_17_1 doi: 10.3390/biom10020320 – ident: e_1_3_4_18_1 doi: 10.3389/fphar.2020.00815 – ident: e_1_3_4_8_1 doi: 10.3389/fphar.2020.00079 – ident: e_1_3_4_7_1 doi: 10.1177/0267659120965921 – ident: e_1_3_4_29_1 doi: 10.1002/jbt.22716 – ident: e_1_3_4_2_1 doi: 10.3389/fneur.2021.609236 – ident: e_1_3_4_36_1 doi: 10.1002/bmc.3273 – ident: e_1_3_4_37_1 doi: 10.3389/fcvm.2021.685434 – ident: e_1_3_4_20_1 doi: 10.1038/s41401-019-0228-6 – ident: e_1_3_4_12_1 doi: 10.1016/j.intimp.2021.107533 – ident: e_1_3_4_31_1 doi: 10.1146/annurev-pharmtox-030620-104842 – ident: e_1_3_4_4_1 doi: 10.1007/s10565-021-09619-8 – ident: e_1_3_4_13_1 doi: 10.1016/j.jep.2018.09.030 – ident: e_1_3_4_15_1 doi: 10.1155/2021/5896931 – ident: e_1_3_4_25_1 doi: 10.1016/j.ejphar.2019.172818 – ident: e_1_3_4_30_1 doi: 10.3390/molecules25225474 – ident: e_1_3_4_32_1 doi: 10.1080/13880209.2020.1849319 – ident: e_1_3_4_10_1 doi: 10.1039/C9FO01984G – ident: e_1_3_4_27_1 doi: 10.1155/2019/9372182 – ident: e_1_3_4_39_1 doi: 10.1080/08982104.2019.1580720 – ident: e_1_3_4_11_1 doi: 10.1016/j.phymed.2019.152885 – ident: e_1_3_4_33_1 doi: 10.3389/fphar.2021.624706 – ident: e_1_3_4_23_1 doi: 10.1152/ajpheart.00155.2018 – ident: e_1_3_4_19_1 doi: 10.3389/fphar.2019.01095 – ident: e_1_3_4_38_1 doi: 10.3389/fphar.2021.666429 – ident: e_1_3_4_9_1 doi: 10.1007/s10741-020-10063-9 – volume: 2015 start-page: 952671 year: 2015 ident: e_1_3_4_6_1 article-title: Shengmai injection improved doxorubicin-induced cardiomyopathy by alleviating myocardial endoplasmic reticulum stress and caspase-12 dependent apoptosis publication-title: Biomed Res Int |
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| Snippet | Shengmai injection (SMI) has been used to treat heart failure.
This study determines the molecular mechanisms of SMI against cardiotoxicity caused by... ContextShengmai injection (SMI) has been used to treat heart failure.ObjectiveThis study determines the molecular mechanisms of SMI against cardiotoxicity... Shengmai injection (SMI) has been used to treat heart failure.CONTEXTShengmai injection (SMI) has been used to treat heart failure.This study determines the... Shengmai injection (SMI) has been used to treat heart failure. This study determines the molecular mechanisms of SMI against cardiotoxicity caused by... Context Shengmai injection (SMI) has been used to treat heart failure.Objective This study determines the molecular mechanisms of SMI against cardiotoxicity... |
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| SubjectTerms | Animals Apoptosis Apoptosis - drug effects Biological Sciences Cardiomyocytes Cardiomyopathy Cardiotoxicity Cardiotoxicity - prevention & control Cells, Cultured Congestive heart failure Creatine Creatine kinase DNA nucleotidylexotransferase DOX Doxorubicin Doxorubicin - toxicity Drug Combinations Drugs, Chinese Herbal - chemistry Drugs, Chinese Herbal - pharmacology heart failure Heme oxygenase (decyclizing) histology Kelch-Like ECH-Associated Protein 1 - chemistry Kelch-Like ECH-Associated Protein 1 - physiology Kinases L-Lactate dehydrogenase Labeling lactate dehydrogenase Lactic acid malondialdehyde Molecular Docking Simulation Molecular modelling mRNA Myocardium - pathology NF-E2-Related Factor 2 - antagonists & inhibitors NF-E2-Related Factor 2 - physiology Nrf2/Keap1 signal pathway oxidative Oxygenase Protein expression Protein folding protein synthesis Proteins Rats Rats, Sprague-Dawley Razoxane Signal transduction Signal Transduction - drug effects Superoxide dismutase Western blotting |
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| Title | In vivo and in vitro protective effects of shengmai injection against doxorubicin-induced cardiotoxicity |
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