Abstract
Objective To explore the effects of the Hedysarum multijugum Maxim.-Radix Salviae compound (Huangqi-Danshen Compound (HDC)) on oxidative capacity and cardiomyocyte apoptosis in rats with diabetic cardiomyopathy by a network pharmacology-based strategy. Methods Traditional Chinese Medicine (TCM)@Taiwan, TCM Systems Pharmacology Database and Analysis Platform (TCMSP), TCM Integrated Database (TCMID), and High-Performance Liquid Chromatography (HPLC) technology were used to obtain and screen HDC's active components, and the PharmMapper database was used to predict HDC human target protein targets. The DCM genes were collected from the GeneCards and OMIM databases, and the network was constructed and analyzed by Cytoscape 3.7.1 and the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Finally, HDC was used to intervene in diabetic cardiomyopathy (DCM) model rats, and important biological processes and signaling pathways were verified using techniques such as immunohistochemistry. Results A total of 176 of HDC's active components and 442 potential targets were obtained. The results of network analysis show that HDC can regulate DCM-related biological processes (such as negative regulation of the apoptotic process, response to hypoxia, the steroid hormone-mediated signaling pathway, cellular iron ion homeostasis, and positive regulation of phosphatidylinositol 3-kinase signaling) and signaling pathways (such as the HIF-1 signaling pathway, the estrogen signaling pathway, insulin resistance, the PPAR signaling pathway, the VEGF signaling pathway, and the PI3K-Akt signaling pathway). Animal experiments show that HDC can reduce fasting plasma glucose (FPG), HbA1c, and malondialdehyde (MDA) and increase superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) (P < 0.05). The results of immunohistochemistry showed that HDC can regulate the protein expression of apoptosis-related signaling pathways in DCM rats (P < 0.05). Conclusion It was initially revealed that HDC improves DCM through its antiapoptotic and anti-inflammatory effects. HDC may play a therapeutic role by improving cardiomyocyte apoptosis in DCM rats.
Highlights
Diabetes is a very common endocrine disease and one of the most common chronic diseases in almost all countries [1].Epidemiological studies show that the number of diabetic patients is increasing year by year
The main mechanism of cardiovascular complications of diabetes is related to the hyperglycemia state and the accumulation of advanced glycation end products, which eventually lead to increased endothelial dysfunction, fibrosis, inflammation, and oxidative stress [5, 7]
Current research indicates that abnormal blood glucose, abnormal blood lipids, left ventricular hypertrophy, metabolic abnormalities, endothelial dysfunction, changes in extracellular matrix of vascular calcification and hypercoagulability, small vascular disease, cardiac autonomic neuropathy, insulin resistance, oxidative stress, and cell metabolism are all important promoters, which are involved in the occurrence and development of Diabetic cardiomyopathy (DCM) [61, 62]
Summary
Diabetes is a very common endocrine disease and one of the most common chronic diseases in almost all countries [1].Epidemiological studies show that the number of diabetic patients is increasing year by year. According to a study by the International Diabetes Federation, the number of diabetic patients has reached 415 million by 2015, and it is estimated. BioMed Research International that the number of diabetic patients will reach 642 million by 2040 [2]. Cardiovascular complications are an important cause of death in patients with diabetes [3, 4]. The main mechanism of cardiovascular complications of diabetes is related to the hyperglycemia state and the accumulation of advanced glycation end products, which eventually lead to increased endothelial dysfunction, fibrosis, inflammation, and oxidative stress [5, 7]. A large number of studies have confirmed that inflammation and oxidative stress play an extremely important role in cardiovascular damage caused by high glucose [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
