Table 2.
Protective Mechanism of Curcumin on Cardiomyocytes
| Research Subjects | Intervention Methods | Mechanism | Refs |
|---|---|---|---|
| SD rats | I/R | I/R-induced oxidative damage is mitigated by activating Sirt1 signaling pathway | [154] |
| Isolated rat heart | I/R | I/R damage is mitigated by activation of the JAK2/STAT3 signaling pathway | [156] |
| SD rats | I/R | I/R damage is mitigated by activation of the JAK2/STAT3 signaling pathway | [157] |
| SD rats | I/R | I/R damage is mitigated by inhibition of TLR2 | [159] |
| H9c2 | I/R | By anti-oxidative stress, inhibition of NF-κB nuclear translocation and JNK phosphorylation | [160] |
| H9c2 | H/R | H/R-induced H9C2 cell damage was alleviated by down-regulating Notch pathway | [161] |
| H9c2 | I/R | I/R damage was mitigated by regulation of total RNA m6A levels | [162] |
| Wistar rat | ISO | Reduce cardiomyocyte apoptosis by preventing excessive mPTP opening | [163] |
| Male Wistar rats | ISO | By increasing the level of Hsp27 | [164] |
| C57BL/6 mice | Hypoxia | Apoptosis was alleviated by miR-7a/b/SP1 pathway | [165] |
| SD rats | CME | Inhibition of TLR4/MyD88/NF-κB signaling pathway alleviates myocardial cell inflammation and apoptosis | [166] |
| Swiss/SV129 mice | Chronic intermittent hypoxia | By inhibiting HIF-1α activation, infarct size is reduced | [167] |
| Neonatal rat cardiomyocytes | Phenylephrine | Cardiomyocyte hypertrophy was alleviated by inhibiting p300-HAT activity | [168] |
| DS rat | High-salt diet | Cardiac hypertrophy was reduced by reducing p300-HAT activity and GATA4 acetylation levels | [169] |
| Adult 129SvEv mice | LPS | Myocardial hypertrophy was alleviated by inhibiting p300-HAT activity | [170] |
| H9c2 cardiomyocytes | Norepinephrine | Cardiomyocyte hypertrophy was inhibited by inhibiting the nuclear localization and DNA binding activity of KATA-4 | [171] |
| Male Wistar rat | TAC | Myocardial hypertrophy was inhibited by upregulation of NCX | [172] |
| SD rat | Nephrectomy, uremia | Myocardial hypertrophy is alleviated by inhibiting GSK-3β/catenin, calcineurin/NFAT and ERK1/2 pathways | [173] |
| Cardiac fibroblasts | TGF-β1 | Myocardial fibrosis is inhibited by inhibition of Smad2/3, p38 MAPK and ERK signaling pathways | [174] |
| Cardiac fibroblasts | TGF-β1 | The expression of α-SMA and collagen was decreased by inhibiting the Smad-2 and p38 MAPK signaling pathways | [175] |
| Cardiac fibroblasts | Ang II | By increasing the expression and activity of PPAR γ, the expression of CTGF, collagen III and FN was inhibited | [176] |
| Cardiac fibroblasts | Ang II | Fibrosis is inhibited by reducing TGF-β1 and MMPs/TIMPs | [177] |
| SD rat | Ang II | By decreasing AT1R expression and enhancing AT2 receptor expression | [178] |
| Cardiac fibroblasts | High glucose | Fibrosis is inhibited by inhibiting TGF-β1/Smad and AMPK/ p38 MAPK signaling pathways | [179] |
| SD rat | I/R | Alleviating myocardial fibrosis by inhibiting TGF-β1/Smad signaling pathway | [180] |
| C57BL/6J mice | MI | Inhibition of fibrosis by activation of Sirt1 | [181] |
| Wistar-Bratislava white rats | ISO | Improved ventricular remodeling by reducing MMP-2 and MMP-9 levels | [182] |
| H9C2 cells | Norepinephrine | By inhibiting the expression and activity of MMP-9 | [183] |
| SD rat | Monocrotaline | RV remodeling was inhibited by decreasing TNF-α levels and oxidative stress | [184] |
| New Zealand rabbits | Capacity and pressure overload | Ventricular remodeling was inhibited by inhibiting P38 and JNK pathways and increasing DKK-3 expression | [185] |
| EAM rats | No-intervention | By inhibiting iNOS, NADPH oxidase and endoplasmic reticulum stress | [186] |
| EAM rats | No-intervention | EAM was weakened by inducing macrophage M2 polarization | [187] |
| SD rat | Streptozotocin, High sugar, high fat diet | By modulating Sirt1/Foxo1 and PI3K/Akt pathways | [188] |
| Male Wistar rats | Streptozotocin, high energy intake | By regulating the Akt/GSK-3β signaling pathway, myocardial fibrosis, oxidative stress, inflammation, and apoptosis are alleviated | [189] |
| Male Wistar rats | Streptozotocin | Curcumin inhibits myocardial fibrosis in diabetic rats by activating Nrf2/HO-1 pathway and inhibiting JAK2/STAT3 pathway | [190] |
| Rats | Streptozotocin | Myocardial hypertrophy was alleviated by inhibiting P300 upregulation | [191] |
| SD rat | Streptozotocin | By activating PPAR γ and inhibiting CaMKII/NF-κB/TGF-β1 pathway | [192] |
| C57BL/KsJ db/db mice | Normal diet | Inflammation is reduced by inhibiting the HMGB1/NLRP3/NF-κB pathway | [193] |
| Diabetic mice | Streptozotocin, high fat diet | Myocardial autophagy in diabetic mice was regulated by AMPK/mTOR pathway | [194] |
| Rats | Dox | Dox-induced cardiotoxicity is mitigated by modulating the Rac1/TWEAK/Fn14/NF-κB complex network | [195] |
| Mice | Dox | The myocardial damage induced by dox was alleviated by up-regulating the expression of 14-3-3γ | [196] |
| Primary rat cardiomyocytes | D-galactose | Autophagy is promoted by increasing Sirt1 expression and phosphorylating AMPK | [197] |
| Wistar rat | 4 to 6 months old | Modulates the TSP1/VEGF-A signaling pathway to promote angiogenesis | [198] |
| Rats | PM2.5 | ERS is inhibited by activation of SERCA2a, thereby improving cardiac inflammation and cardiomyocyte apoptosis | [199] |