Sample Type | n | Range | Average |
---|---|---|---|
Serum | 5 | 93% - 98% | 96% |
EDTA Plasma | 5 | 86% - 102% | 95% |
Heparin Plasma | 5 | 91% - 103% | 99% |
Sample Type | n | 1:2 | 1:4 | 1:8 |
---|---|---|---|---|
Serum | 5 | 86-100% | 85-101% | 88-104% |
EDTA Plasma | 5 | 82-101% | 86-93% | 83-100% |
Heparin Plasma | 5 | 80-97% | 82-99% | 80-100% |
Item | Quantity | Storage |
---|---|---|
Pre-Coated 96 Well Microplate | 12 x 8 Well Strips | +4°C |
Lyopholized Standard | 2 Vials | +4°C |
Sample Dilution Buffer | 20ml | +4°C |
Biotinylated Detection Antibody | 120µl | +4°C |
Antibody Dilution Buffer | 10ml | +4°C |
HRP-Streptavidin Conjugate | 120µl | +4°C |
SABC Dilution Buffer | 10ml | +4°C |
TMB Substrate | 10ml | +4°C |
Stop Solution | 10ml | +4°C |
Wash Buffer (25X) | 30ml | +4°C |
Plate Sealers | 5 Adhesive Strips | - |
Foil Pouch | 1 Zip-Sealed Pouch | - |
Myocardial fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix in myocardial interstitial spaces. Myocardial fibrosis is a fundamental process in ventricular remodeling and a primary contributor to the progression of heart failure. Liquiritigenin (LQ) is a flavanone compound with anti-oxidative, anti-carcinogenic, anti-inflammatory and estrogenic properties. The present study aimed to investigate the regulatory potential of LQ treatment in a mouse model of isoprenaline (ISO)-induced cardiac fibrosis and in cultured H9C2 cardiomyocytes stimulated with angiotensin II (Ang II). The treatment of ISO-induced mice with LQ significantly decreased the levels of cardiac injury-related proteins in the serum and ECM accumulation in mouse heart tissues. LQ treatment also effectively alleviated cardiac dysfunction in ISO-treated mice. Further analyses revealed that LQ inhibited ISO-induced collagen formation and activation of the transforming growth factor-ß1 (TGF-ß1)/Smad2 and protein kinase B (AKT)/extracellular signal-regulated kinase (ERK) signaling pathways. As a major pathological event in myocardial fibrosis, the apoptosis of cardiomyocytes has been considered a key mechanism contributing to impaired left ventricle performance. The pretreatment of rat cardiomyocytes with LQ significantly reduced the apoptosis of H9C2 cells, and inhibited Ang II-induced activation of the TGF-ß1/Smad2 and AKT/ERK pathways. In conclusion, the present study revealed that LQ ameliorated ISO-induced myocardial fibrosis in mice and inhibited the apoptosis of cardiomyocytes in vitro by inhibiting the TGF-ß1/Smad2 and AKT/ERK signaling pathways. These results suggested the anti-fibrotic and cardioprotective potential of LQ in fibrosis, thus supporting the use of LQ for the management of cardiomyocyte injury and myocardial fibrosis in patients with cardiac diseases.