FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3201943150> ?p ?o ?g. }

• W3201943150 endingPage "16" @default.
• W3201943150 startingPage "1" @default.
• W3201943150 abstract "The pathogenesis and clinical features of diabetic cardiomyopathy (DCM) have been well studied in the past decade; however, effective approaches to prevent and treat this disease are limited. Fufang Zhenzhu Tiaozhi (FTZ) formula, a traditional Chinese prescription, is habitually used to treat dyslipidemia and diabetes. Recently, several studies have reported the therapeutic effects of FTZ on cardiovascular diseases. However, the effects of FTZ on DCM have not yet been fully elucidated. This study investigated the effects of FTZ on DCM and determined the mechanisms underlying its efficacy.Diabetes was induced in mice by intraperitoneal injection of streptozotocin; the mice were randomly divided into a control group (Con), diabetes group (DCM), and diabetes-treated with FTZ (DCM + FTZ). Myocardial structural alterations, fibrosis biomarkers, and inflammation were observed. Besides, the potential targets and their related signaling pathways were analyzed using network pharmacology and further verified by Western blot.Diabetic mice showed significant body weight loss, hyperglycemia, and excessive collagen content in the cardiac tissue, while serum and myocardial inflammatory factors significantly increased. Nerveless, treatment with FTZ for 1 month significantly improved body weight, attenuated hyperglycemia, and alleviated diabetes-associated myocardial structure and function abnormalities. Furthermore, the serum levels of interleukin 12 (IL-12) and chemokine (C-C motif) ligand 2 (CCL2) as well as the mRNA levels of cardiac IL-12, IL-6, and C-C motif chemokine receptor 2 (Ccr2) reduced after FTZ treatment. Additionally, a total of 67 active compounds and 76 potential targets related to DCM were analyzed. Pathway and functional enrichment analyses showed that FTZ mainly regulates inflammation-related pathways, including MAPK and PI3K-AKT signaling pathways. Further investigation revealed that the activities of STAT3, AKT, and ERK were augmented in diabetic hearts but decreased in FTZ-treated cardiac tissues.Our results suggest that FTZ exhibits therapeutic properties against DCM by ameliorating hyperglycemia-induced inflammation and fibrosis via at least partial inhibition of AKT, ERK, and STAT3 signaling pathways." @default.
• W3201943150 created "2021-10-11" @default.
• W3201943150 creator A5000033522 @default.
• W3201943150 creator A5001197883 @default.
• W3201943150 creator A5007768703 @default.
• W3201943150 creator A5008034788 @default.
• W3201943150 creator A5011756100 @default.
• W3201943150 creator A5023932055 @default.
• W3201943150 creator A5031368100 @default.
• W3201943150 creator A5035149095 @default.
• W3201943150 creator A5055947638 @default.
• W3201943150 creator A5069767459 @default.
• W3201943150 date "2021-09-28" @default.
• W3201943150 modified "2023-10-18" @default.
• W3201943150 title "FTZ Ameliorates Diabetic Cardiomyopathy by Inhibiting Inflammation and Cardiac Fibrosis in the Streptozotocin-Induced Model" @default.
• W3201943150 cites W2011114112 @default.
• W3201943150 cites W2011467994 @default.
• W3201943150 cites W2045824542 @default.
• W3201943150 cites W2046989141 @default.
• W3201943150 cites W2060235241 @default.
• W3201943150 cites W2067970312 @default.
• W3201943150 cites W2077866526 @default.
• W3201943150 cites W2087187911 @default.
• W3201943150 cites W2095521683 @default.
• W3201943150 cites W2100238813 @default.
• W3201943150 cites W2115532337 @default.
• W3201943150 cites W2124679671 @default.
• W3201943150 cites W2145461802 @default.
• W3201943150 cites W2151155970 @default.
• W3201943150 cites W2158038801 @default.
• W3201943150 cites W2163388642 @default.
• W3201943150 cites W2223495077 @default.
• W3201943150 cites W2279201083 @default.
• W3201943150 cites W2362635822 @default.
• W3201943150 cites W2407918174 @default.
• W3201943150 cites W2591558322 @default.
• W3201943150 cites W2596947530 @default.
• W3201943150 cites W2608644283 @default.
• W3201943150 cites W2614910789 @default.
• W3201943150 cites W2620784243 @default.
• W3201943150 cites W2744809834 @default.
• W3201943150 cites W2756104041 @default.
• W3201943150 cites W2766193612 @default.
• W3201943150 cites W2772652485 @default.
• W3201943150 cites W2792012916 @default.
• W3201943150 cites W2806662788 @default.
• W3201943150 cites W2810359819 @default.
• W3201943150 cites W2836826811 @default.
• W3201943150 cites W2883039929 @default.
• W3201943150 cites W2890766099 @default.
• W3201943150 cites W2895498913 @default.
• W3201943150 cites W2901585229 @default.
• W3201943150 cites W2902557478 @default.
• W3201943150 cites W2909750767 @default.
• W3201943150 cites W2910926942 @default.
• W3201943150 cites W2914104637 @default.
• W3201943150 cites W2917376005 @default.
• W3201943150 cites W2919163899 @default.
• W3201943150 cites W2925683344 @default.
• W3201943150 cites W2937067600 @default.
• W3201943150 cites W2940275338 @default.
• W3201943150 cites W2947490932 @default.
• W3201943150 cites W2948394063 @default.
• W3201943150 cites W2953485758 @default.
• W3201943150 cites W2953978988 @default.
• W3201943150 cites W2954711096 @default.
• W3201943150 cites W2958198050 @default.
• W3201943150 cites W2958607853 @default.
• W3201943150 cites W2960054618 @default.
• W3201943150 cites W2965631439 @default.
• W3201943150 cites W2969719427 @default.
• W3201943150 cites W2970695160 @default.
• W3201943150 cites W2971469202 @default.
• W3201943150 cites W2985310880 @default.
• W3201943150 cites W2989860256 @default.
• W3201943150 cites W2991152880 @default.
• W3201943150 cites W3005271349 @default.
• W3201943150 cites W3006949946 @default.
• W3201943150 cites W3034098824 @default.
• W3201943150 cites W3088080395 @default.
• W3201943150 cites W330316361 @default.
• W3201943150 cites W4285719527 @default.
• W3201943150 cites W4292400027 @default.
• W3201943150 cites W978308701 @default.
• W3201943150 doi "https://doi.org/10.1155/2021/5582567" @default.
• W3201943150 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8492284" @default.
• W3201943150 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34621323" @default.
• W3201943150 hasPublicationYear "2021" @default.
• W3201943150 type Work @default.
• W3201943150 sameAs 3201943150 @default.
• W3201943150 citedByCount "9" @default.
• W3201943150 countsByYear W32019431502022 @default.
• W3201943150 crossrefType "journal-article" @default.
• W3201943150 hasAuthorship W3201943150A5000033522 @default.
• W3201943150 hasAuthorship W3201943150A5001197883 @default.
• W3201943150 hasAuthorship W3201943150A5007768703 @default.
• W3201943150 hasAuthorship W3201943150A5008034788 @default.
• W3201943150 hasAuthorship W3201943150A5011756100 @default.

• next