Table 1.
Pharmacological effects of emodin in anti-cardiovascular diseases.
| References | Finding | Methodology |
|---|---|---|
| Immunomodulation | ||
| (Wu et al., 2007) | TNF-α↓, NF-κB inhibited, caspase-3 inhibited | Emodin treatment in BALB/c mice with AMI |
| (Song et al., 2012) | TNF-α and IL-1β↓, NF-κBp65 inhibited | Emodin treatment in EAM in male Lewis rats |
| (Jiang et al., 2014) | IL-1β, IL-6, TNF-α, IL-23, and IL-17↓, NF-κBp65 inhibited | Emodin treatment in BALB/c mice with viral myocarditis |
| (Shou et al., 2018) | PPAR-γ and eNOS phosphorylation↑, NO↑ | Emodin treatment in HAECs with ischemia-mimetic |
| (Xu et al., 2018b) | BMP2, TRAF1, and RELA↓, calcification, and phenotypical transformation of hVICs via the NF-κB signaling pathway | Emodin treatment in calcification of human aortic valve interstitial cells |
| (Yang et al., 2019) | IL-1β, IL-6, TNF-α, and↓, miR-223↓, cell viability, and cyclinD1↑, apoptosis was suppressed, Jnk signaling pathway inhibited by miR-223 | Emodin treatment in H9c2 cells with myocarditis |
| Anti-apoptosis | ||
| (Liu et al., 2013) | caspase-3↓, Bcl-2↑ | Emodin treatment in BALB/c mice and HEp-2 cells with viral myocarditis |
| (Zhang et al., 2019) | miR-138↑, MLK3↓, p53 and p21↓, cyclin D1↑, caspase-3 and caspase-9↓Sirt1/AKT, and Wnt/β-catenin pathways activated, | Emodin treatment in H9c2 cells with myocardial ischemia |
| (Huang et al., 2019) | miR‐26a↓, survivin↑, caspase-3, and caspase-9↓, JAK1/STAT3 signal activated | Emodin treatment in H9c2 cells with myocardial ischemia |
| (Ye et al., 2019) | GSDMD-N↓, IL-1β↓, TLR4/MyD88/NF-κB/NLRP3 inhibited | Emodin treatment in Sprague-Dawley rats cardiomyocytes with ischemia/reperfusion injury |
| Anti-myocardial fibrosis | ||
| (Xiao et al., 2019) | MTA3↑, COL1A2, and α-SMA↓ | Emodin treatment in mouse model of pathological cardiac hypertrophy with excess fibrosis |
| Anti-cardiac hypertrophy | ||
| (Evans et al., 2020) | I HDAC and II HDAC activity inhibited, histone acetylation in cardiomyocytes↑, ERK phosphorylation inhibited | Emodin treatment in C57BL/6 mice with cardiac hypertrophy (transverse aortic constriction-induced) and fibrosis (AngII-induced) |
| (Gao et al., 2020) | SIRT3↑, modulation of mitochondrial SIRT3 and its downstream signaling pathway | Emodin treatment or prevent in H9c2 cells with hypertrophy, primary cultured cardiomyocytes, and WT C57BL/6 mice and SIRT3-KO mice with cardiac hypertrophy |
| Anti-oxidative damage | ||
| (Du and Ko, 2005) | ATP↑, myocardial mitochondrial SOD activity in female↑ | Emodin pretreatment Sprague-Dawley isolated rat hearts (male and female) with I-R injury |
| (Du and Ko, 2006) | LDH leakage↓, mitochondrial antioxidant components↑, contractile force recovery↑ | Emodin pretreatment Sprague-Dawley isolated rat hearts with I-R injury |
| Anti-proliferative | ||
| (Wang X. et al., 2007) | damages DNA, production of ROS and expression of p53↑, VSMCs proliferation inhibited | Emodin treatment in abnormal proliferation and migration of VSMC |
| (Wang S. J. et al., 2008) | VSMCs proliferation inhibited | Emodin on VSMCs proliferation induced by Ang II |
| Other pathways and functions | ||
| (Zhou et al., 2014) | ANP↑, L-type Ca (2+) channels inhibited, K (+) ATP channel activated | Emodin treatment in isolated perfused beating rabbit atria |
| (Chen et al., 2014) | MMP-2 and TIMP-2 expression↓ | Emodin treatment in hypertensive rats with LV fibrosis in Goldblatt (2K1C) |
| (Wu et al., 2014) | Improve diabetes-induced systolic dysfunction. Akt and GSK-3β phosphorylation↑, HR↑, LVESD, LWPWT, and IVSD ↓. | Emodin treatment in Wistar rats with diabetic cardiomyopathy |
| (Nemmar et al., 2015) | Leukocytes, erythrocytes, hematocrit, and hemoglobin concentrations↓, IL-1β and TNF-α↓, antioxidant activities SOD and GR↑, shortening of the PT and aPTT reversed | Emodin treatment in Tuck-Ordinary mice with cardiac inflammation and oxidative stress |