Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder
Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-11, Vol.50 (5), p.1726-1739 |
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| creator | Tian, Jing Tang, Wenzhu Xu, Ming Zhang, Chen Zhao, Pei Cao, Tongtong Shan, Xiaoli Lu, Rong Guo, Wei |
| description | Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism. |
| doi_str_mv | 10.1159/000494791 |
| format | Article |
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In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000494791</identifier><identifier>PMID: 30384366</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>AMP-Activated Protein Kinases - metabolism ; Animals ; Cardiomyopathy ; Diabetes ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - pathology ; Diabetes Mellitus, Type 2 - veterinary ; Diabetic Cardiomyopathies - drug therapy ; Diabetic Cardiomyopathies - etiology ; Diabetic Cardiomyopathies - pathology ; Diabetic cardiomyopathy ; Diet ; Drugs, Chinese Herbal - pharmacology ; Drugs, Chinese Herbal - therapeutic use ; Fatty acids ; Glucose ; Heart ; Homeostasis ; Lipids ; Male ; Metabolic disorders ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Myocardium - metabolism ; Myocardium - pathology ; Myocytes, Cardiac - cytology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Nuclear Respiratory Factor 1 - metabolism ; Obesity ; Original Paper ; Oxidative Phosphorylation - drug effects ; Oxidative stress ; Palmitic Acid - pharmacology ; Peroxisome proliferator-activated receptor gamma coactivator 1-alpha ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Phosphorylation ; Proteins ; Receptors, Leptin - deficiency ; Receptors, Leptin - genetics ; Shengmai San ; Signal Transduction - drug effects ; Sirtuin 1 - metabolism ; Uncoupling Protein 2 - metabolism</subject><ispartof>Cellular physiology and biochemistry, 2018-11, Vol.50 (5), p.1726-1739</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-cc029d07618a8a9b113e01e6f635f42661ccfc131ecfe0ef7d481c3fcb7d8f8b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2096,27612,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30384366$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tian, Jing</creatorcontrib><creatorcontrib>Tang, Wenzhu</creatorcontrib><creatorcontrib>Xu, Ming</creatorcontrib><creatorcontrib>Zhang, Chen</creatorcontrib><creatorcontrib>Zhao, Pei</creatorcontrib><creatorcontrib>Cao, Tongtong</creatorcontrib><creatorcontrib>Shan, Xiaoli</creatorcontrib><creatorcontrib>Lu, Rong</creatorcontrib><creatorcontrib>Guo, Wei </creatorcontrib><title>Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism.</description><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>Cardiomyopathy</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes Mellitus, Type 2 - veterinary</subject><subject>Diabetic Cardiomyopathies - drug therapy</subject><subject>Diabetic Cardiomyopathies - etiology</subject><subject>Diabetic Cardiomyopathies - pathology</subject><subject>Diabetic cardiomyopathy</subject><subject>Diet</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Drugs, Chinese Herbal - therapeutic use</subject><subject>Fatty acids</subject><subject>Glucose</subject><subject>Heart</subject><subject>Homeostasis</subject><subject>Lipids</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Myocytes, Cardiac - cytology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Nuclear Respiratory Factor 1 - metabolism</subject><subject>Obesity</subject><subject>Original Paper</subject><subject>Oxidative Phosphorylation - drug effects</subject><subject>Oxidative stress</subject><subject>Palmitic Acid - pharmacology</subject><subject>Peroxisome proliferator-activated receptor gamma coactivator 1-alpha</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Receptors, Leptin - deficiency</subject><subject>Receptors, Leptin - genetics</subject><subject>Shengmai San</subject><subject>Signal Transduction - drug effects</subject><subject>Sirtuin 1 - metabolism</subject><subject>Uncoupling Protein 2 - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNpdkUtv1DAURiMEoqWwYI-QpW5gEbBjx49lNeUx0lQsWtaWY19PPCTxYCeV5t_jMsMsWPnaOvfIn76qekvwJ0Ja9RljzBQTijyrLglrSK2EkM_LjElbSyXFRfUq5x0uV6Gal9UFxVQyyvllNd73MG1HE9C9mdDNMMBjMDNkdBtMB3OwaGWSC3E8xL2Z-wN66FNctj1aj_sUH2GEaUbRo7swR9vHyaVgBrQJ--DQHcymi0Nx3IYck4P0unrhzZDhzem8qn5-_fKw-l5vfnxbr242tWW0nWtrcaMcFpxII43qCKGACXDPaetZwzmx1ltCCVgPGLxwTBJLve2Ek1529KpaH70ump3epzCadNDRBP33IaatNqmEG0B3zvpGKGY5Leq2M85zIRi1zgF0_sn14egqeX8vkGc9hmxhGMwEccm6IY1qqWCMF_T6P3QXlzSVpLqhmMjSUasK9fFI2RRzTuDPHyRYP_Wpz30W9v3JuHQjuDP5r8ACvDsCv0zaQjoDp_0_0cOlBQ</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Tian, Jing</creator><creator>Tang, Wenzhu</creator><creator>Xu, Ming</creator><creator>Zhang, Chen</creator><creator>Zhao, Pei</creator><creator>Cao, Tongtong</creator><creator>Shan, Xiaoli</creator><creator>Lu, Rong</creator><creator>Guo, Wei </creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20181101</creationdate><title>Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder</title><author>Tian, Jing ; Tang, Wenzhu ; Xu, Ming ; Zhang, Chen ; Zhao, Pei ; Cao, Tongtong ; Shan, Xiaoli ; Lu, Rong ; Guo, Wei </author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-cc029d07618a8a9b113e01e6f635f42661ccfc131ecfe0ef7d481c3fcb7d8f8b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Animals</topic><topic>Cardiomyopathy</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes Mellitus, Type 2 - veterinary</topic><topic>Diabetic Cardiomyopathies - drug therapy</topic><topic>Diabetic Cardiomyopathies - etiology</topic><topic>Diabetic Cardiomyopathies - pathology</topic><topic>Diabetic cardiomyopathy</topic><topic>Diet</topic><topic>Drugs, Chinese Herbal - pharmacology</topic><topic>Drugs, Chinese Herbal - therapeutic use</topic><topic>Fatty acids</topic><topic>Glucose</topic><topic>Heart</topic><topic>Homeostasis</topic><topic>Lipids</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Myocytes, Cardiac - cytology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Nuclear Respiratory Factor 1 - metabolism</topic><topic>Obesity</topic><topic>Original Paper</topic><topic>Oxidative Phosphorylation - drug effects</topic><topic>Oxidative stress</topic><topic>Palmitic Acid - pharmacology</topic><topic>Peroxisome proliferator-activated receptor gamma coactivator 1-alpha</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Receptors, Leptin - deficiency</topic><topic>Receptors, Leptin - genetics</topic><topic>Shengmai San</topic><topic>Signal Transduction - drug effects</topic><topic>Sirtuin 1 - metabolism</topic><topic>Uncoupling Protein 2 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tian, Jing</creatorcontrib><creatorcontrib>Tang, Wenzhu</creatorcontrib><creatorcontrib>Xu, Ming</creatorcontrib><creatorcontrib>Zhang, Chen</creatorcontrib><creatorcontrib>Zhao, Pei</creatorcontrib><creatorcontrib>Cao, Tongtong</creatorcontrib><creatorcontrib>Shan, Xiaoli</creatorcontrib><creatorcontrib>Lu, Rong</creatorcontrib><creatorcontrib>Guo, Wei </creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tian, Jing</au><au>Tang, Wenzhu</au><au>Xu, Ming</au><au>Zhang, Chen</au><au>Zhao, Pei</au><au>Cao, Tongtong</au><au>Shan, Xiaoli</au><au>Lu, Rong</au><au>Guo, Wei </au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-11-01</date><risdate>2018</risdate><volume>50</volume><issue>5</issue><spage>1726</spage><epage>1739</epage><pages>1726-1739</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. Methods: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined. Myocardial ultrastructural morphology was observed with transmission electron microscopy. Protein expression and activity of oxidative phosphorylation (OXPHOS) complex were assessed using western blotting and microplate assay kits. We also observed cellular viability, mitochondrial membrane potential, OXPHOS complex activity, and cellular ATP level in palmitic acid-stimulated H9C2 cardiomyocytes. Changes in the sirtuin (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway and mitochondrial uncoupling signaling were assessed using western blotting and quantitative real-time PCR. Results: Leptin receptor-deficient db/db mice exhibit obesity, hyperglycemia, and hyperlipidemia, accompanied by distinct myocardial hypertrophy and diastolic dysfunction. SMS at a dose of 3 g/kg body weight contributed to a recovery of diabetes-induced myocardial hypertrophy and diastolic dysfunction. SMS administration led to an effective restoration of mitochondrial structure and function both in vivo and in vitro. Furthermore, SMS markedly enhanced SIRT1 and p-AMPKα protein levels and decreased the expression of acetylated-PGC-1α and uncoupling protein 2 protein. SMS also restored the depletion of NRF1 and TFAM levels in diabetic hearts and H9C2 cardiomyocytes. Conclusion: The results indicate that SMS may alleviate diabetes-induced myocardial hypertrophy and diastolic dysfunction by improving mitochondrial lipid metabolism.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30384366</pmid><doi>10.1159/000494791</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AMP-Activated Protein Kinases - metabolism Animals Cardiomyopathy Diabetes Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - veterinary Diabetic Cardiomyopathies - drug therapy Diabetic Cardiomyopathies - etiology Diabetic Cardiomyopathies - pathology Diabetic cardiomyopathy Diet Drugs, Chinese Herbal - pharmacology Drugs, Chinese Herbal - therapeutic use Fatty acids Glucose Heart Homeostasis Lipids Male Metabolic disorders Mice Mice, Inbred C57BL Mice, Knockout Mitochondria Mitochondria - drug effects Mitochondria - metabolism Myocardium - metabolism Myocardium - pathology Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Nuclear Respiratory Factor 1 - metabolism Obesity Original Paper Oxidative Phosphorylation - drug effects Oxidative stress Palmitic Acid - pharmacology Peroxisome proliferator-activated receptor gamma coactivator 1-alpha Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Phosphorylation Proteins Receptors, Leptin - deficiency Receptors, Leptin - genetics Shengmai San Signal Transduction - drug effects Sirtuin 1 - metabolism Uncoupling Protein 2 - metabolism |
| title | Shengmai San Alleviates Diabetic Cardiomyopathy Through Improvement of Mitochondrial Lipid Metabolic Disorder |
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