The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain
Aim3,4-Dihydroxyl-phenyl lactic acid (DLA) and notoginsenoside R1 (R1) are known to protect ischemia and reperfusion (I/R) injury by targeting Sirtuin1/NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 10/the Mitochondrial Complex I (Sirt-1/NDUFA10/Complex I) and Rho-associated kinase/adenosine tri...
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Frontiers Media S.A.
2021-07-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2021.538962/full |
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| author | Li Yan Li Yan Li Yan Li Yan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Bai-He Hu Bai-He Hu Bai-He Hu Bai-He Hu Xin Chang Xin Chang Xin Chang Xin Chang Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Ping Huang Ping Huang Ping Huang Ping Huang Jian Liu Jian Liu Jian Liu Jian Liu Jian Liu Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Quan Li Quan Li Quan Li Quan Li Kai Sun Kai Sun Kai Sun Kai Sun Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Ke He Ke He Ke He Ke He Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han |
| author_facet | Li Yan Li Yan Li Yan Li Yan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Bai-He Hu Bai-He Hu Bai-He Hu Bai-He Hu Xin Chang Xin Chang Xin Chang Xin Chang Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Ping Huang Ping Huang Ping Huang Ping Huang Jian Liu Jian Liu Jian Liu Jian Liu Jian Liu Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Quan Li Quan Li Quan Li Quan Li Kai Sun Kai Sun Kai Sun Kai Sun Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Ke He Ke He Ke He Ke He Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han |
| author_sort | Li Yan |
| collection | DOAJ |
| description | Aim3,4-Dihydroxyl-phenyl lactic acid (DLA) and notoginsenoside R1 (R1) are known to protect ischemia and reperfusion (I/R) injury by targeting Sirtuin1/NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 10/the Mitochondrial Complex I (Sirt-1/NDUFA10/Complex I) and Rho-associated kinase/adenosine triphosphate (ROCK/ATP) ATP synthase δ subunit (ATP 5D), respectively. We hypothesized that a composite of the two may exhibit a more potent effect on I/R injury. The study was designed to test this hypothesis.Materials and MethodsMale Sprague–Dawley rats underwent left anterior descending artery occlusion and reperfusion, with or without DLA, R1, or a combination of 3,4-dihydroxyl-phenyl lactic acid and notoginsenoside R1 (DR) pretreatment. Heart function, myocardial morphology, myocardial infarct, myocardial blood flow (MBF), apoptosis, vascular diameter, and red blood cell (RBC) velocity in venules were evaluated. Myeloperoxidase (MPO), malondialdehyde (MDA), and 8-oxo-deoxyguanosine (8-OHdG) were assessed. The content of ATP, adenosine diphosphate (ADP), and adenosine monophosphate (AMP), the activity of mitochondrial respiratory chain Complex I and its subunit NDUFA10, the Mitochondrial Complex V (Complex V) and its subunit ATP 5D, Sirt-1, Ras homolog gene family, member A (RhoA), ROCK-1, and phosphorylated myosin light chain (P-MLC) were evaluated. R1 binding to Sirt-1 was determined by surface plasmon resonance.ResultsDLA inhibited the expression of Sirt-1, the reduction in Complex I activity and its subunit NDUFA10 expression, the increase in MPO, MDA, and 8-OhdG, and apoptosis. R1 inhibited the increase in the expression of RhoA/ROCK-1/P-MLC, the reduction of Complex V activity and its subunit ATP 5D expression, alleviated F-actin, and myocardial fiber rupture. Both DLA and R1 reduced the myocardial infarction size, increased the velocities of RBC in venules, and improved MBF and heart function impaired by I/R. DR exhibited effects similar to what was exerted, respectively, by DLA and R1 in terms of respiratory chain complexes and related signaling and outcomes, and an even more potent effect on myocardial infarct size, RBC velocity, heart function, and MBF than DLA and R1 alone.ConclusionA combination of 3,4-dihydroxyl-phenyl lactic acid and notoginsenoside R1 revealed a more potent effect on I/R injury via the additive effect of DLA and R1, which inhibited not only apoptosis caused by low expression of Sirt-1/NDUFA10/Complex I but also myocardial fiber fracture caused by RhoA/ROCK-1 activation and decreased expression of ATP/ATP 5D/Complex V. |
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| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-12-22T15:56:33Z |
| publishDate | 2021-07-01 |
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| series | Frontiers in Physiology |
| spelling | doaj.art-40ed6f3e2b8046d9a340ad40f4c51d622022-12-21T18:20:47ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2021-07-011210.3389/fphys.2021.538962538962The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory ChainLi Yan0Li Yan1Li Yan2Li Yan3Chun-Shui Pan4Chun-Shui Pan5Chun-Shui Pan6Chun-Shui Pan7Yu-Ying Liu8Yu-Ying Liu9Yu-Ying Liu10Yu-Ying Liu11Yuan-Chen Cui12Yuan-Chen Cui13Yuan-Chen Cui14Yuan-Chen Cui15Bai-He Hu16Bai-He Hu17Bai-He Hu18Bai-He Hu19Xin Chang20Xin Chang21Xin Chang22Xin Chang23Xiao-Hong Wei24Xiao-Hong Wei25Xiao-Hong Wei26Xiao-Hong Wei27Ping Huang28Ping Huang29Ping Huang30Ping Huang31Jian Liu32Jian Liu33Jian Liu34Jian Liu35Jian Liu36Jing-Yu Fan37Jing-Yu Fan38Jing-Yu Fan39Jing-Yu Fan40Quan Li41Quan Li42Quan Li43Quan Li44Kai Sun45Kai Sun46Kai Sun47Kai Sun48Lu-Lu Yan49Lu-Lu Yan50Lu-Lu Yan51Lu-Lu Yan52Ke He53Ke He54Ke He55Ke He56Jing-Yan Han57Jing-Yan Han58Jing-Yan Han59Jing-Yan Han60Jing-Yan Han61Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaDepartment of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaTasly Microcirculation Research Center, Peking University Health Science Center, Beijing, ChinaDepartment of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, ChinaKey Laboratory of Stasis and Phlegm, State Administration of Traditional Chinese Medicine of the People’s Republic of China, Beijing, ChinaState Key Laboratory of Core Technology in Innovative Chinese Medicine, Tianjin, ChinaBeijing Microvascular Institute of Intergration of Chinese and Western Medicine, Beijing, ChinaAim3,4-Dihydroxyl-phenyl lactic acid (DLA) and notoginsenoside R1 (R1) are known to protect ischemia and reperfusion (I/R) injury by targeting Sirtuin1/NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 10/the Mitochondrial Complex I (Sirt-1/NDUFA10/Complex I) and Rho-associated kinase/adenosine triphosphate (ROCK/ATP) ATP synthase δ subunit (ATP 5D), respectively. We hypothesized that a composite of the two may exhibit a more potent effect on I/R injury. The study was designed to test this hypothesis.Materials and MethodsMale Sprague–Dawley rats underwent left anterior descending artery occlusion and reperfusion, with or without DLA, R1, or a combination of 3,4-dihydroxyl-phenyl lactic acid and notoginsenoside R1 (DR) pretreatment. Heart function, myocardial morphology, myocardial infarct, myocardial blood flow (MBF), apoptosis, vascular diameter, and red blood cell (RBC) velocity in venules were evaluated. Myeloperoxidase (MPO), malondialdehyde (MDA), and 8-oxo-deoxyguanosine (8-OHdG) were assessed. The content of ATP, adenosine diphosphate (ADP), and adenosine monophosphate (AMP), the activity of mitochondrial respiratory chain Complex I and its subunit NDUFA10, the Mitochondrial Complex V (Complex V) and its subunit ATP 5D, Sirt-1, Ras homolog gene family, member A (RhoA), ROCK-1, and phosphorylated myosin light chain (P-MLC) were evaluated. R1 binding to Sirt-1 was determined by surface plasmon resonance.ResultsDLA inhibited the expression of Sirt-1, the reduction in Complex I activity and its subunit NDUFA10 expression, the increase in MPO, MDA, and 8-OhdG, and apoptosis. R1 inhibited the increase in the expression of RhoA/ROCK-1/P-MLC, the reduction of Complex V activity and its subunit ATP 5D expression, alleviated F-actin, and myocardial fiber rupture. Both DLA and R1 reduced the myocardial infarction size, increased the velocities of RBC in venules, and improved MBF and heart function impaired by I/R. DR exhibited effects similar to what was exerted, respectively, by DLA and R1 in terms of respiratory chain complexes and related signaling and outcomes, and an even more potent effect on myocardial infarct size, RBC velocity, heart function, and MBF than DLA and R1 alone.ConclusionA combination of 3,4-dihydroxyl-phenyl lactic acid and notoginsenoside R1 revealed a more potent effect on I/R injury via the additive effect of DLA and R1, which inhibited not only apoptosis caused by low expression of Sirt-1/NDUFA10/Complex I but also myocardial fiber fracture caused by RhoA/ROCK-1 activation and decreased expression of ATP/ATP 5D/Complex V.https://www.frontiersin.org/articles/10.3389/fphys.2021.538962/full34-dihydroxyl-phenyl lactic acidnotoginsenoside R1myocardium ischemia reperfusion injuryComplex IComplex V |
| spellingShingle | Li Yan Li Yan Li Yan Li Yan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Chun-Shui Pan Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yu-Ying Liu Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Yuan-Chen Cui Bai-He Hu Bai-He Hu Bai-He Hu Bai-He Hu Xin Chang Xin Chang Xin Chang Xin Chang Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Xiao-Hong Wei Ping Huang Ping Huang Ping Huang Ping Huang Jian Liu Jian Liu Jian Liu Jian Liu Jian Liu Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Jing-Yu Fan Quan Li Quan Li Quan Li Quan Li Kai Sun Kai Sun Kai Sun Kai Sun Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Lu-Lu Yan Ke He Ke He Ke He Ke He Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han Jing-Yan Han The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain Frontiers in Physiology 3 4-dihydroxyl-phenyl lactic acid notoginsenoside R1 myocardium ischemia reperfusion injury Complex I Complex V |
| title | The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain |
| title_full | The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain |
| title_fullStr | The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain |
| title_full_unstemmed | The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain |
| title_short | The Composite of 3, 4-Dihydroxyl-Phenyl Lactic Acid and Notoginsenoside R1 Attenuates Myocardial Ischemia and Reperfusion Injury Through Regulating Mitochondrial Respiratory Chain |
| title_sort | composite of 3 4 dihydroxyl phenyl lactic acid and notoginsenoside r1 attenuates myocardial ischemia and reperfusion injury through regulating mitochondrial respiratory chain |
| topic | 3 4-dihydroxyl-phenyl lactic acid notoginsenoside R1 myocardium ischemia reperfusion injury Complex I Complex V |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2021.538962/full |
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yuyingliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuyingliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuyingliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuanchencui compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuanchencui compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuanchencui compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT yuanchencui compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT baihehu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT baihehu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT baihehu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT baihehu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xinchang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xinchang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xinchang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xinchang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xiaohongwei compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xiaohongwei compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xiaohongwei compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT xiaohongwei compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT pinghuang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT pinghuang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT pinghuang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT pinghuang compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jianliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jianliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jianliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jianliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jianliu compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyufan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyufan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyufan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyufan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT quanli compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT quanli compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT quanli compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT quanli compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kaisun compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kaisun compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kaisun compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kaisun compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT luluyan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT luluyan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT luluyan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT luluyan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kehe compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kehe compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kehe compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT kehe compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyanhan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyanhan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyanhan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyanhan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain AT jingyanhan compositeof34dihydroxylphenyllacticacidandnotoginsenosider1attenuatesmyocardialischemiaandreperfusioninjurythroughregulatingmitochondrialrespiratorychain |