Table 2.

Summarized the effects and mechanisms of ginsenoside Rg1 Protective effect on ischemic cardiomyocytes.

Primary Action	Experimental models	Specific Effects	Mechanisms	Ref
Improve myocardial injury	ISO-induced AMI rats	Improve oxidative stress and inflammation, inhibit cardiomyocyte apoptosis	Inhibit PTEN expression thereby activating PI3K/Akt pathway	[69]
	I/R-induced H9c2 cells	Reduce ROS and MDA production, increase antioxidant enzyme levels	Activate Nrf2 and HO-1	[71]
	LPS or H/R-induced H9C2 cells	Inhibit mitochondrial Ca2+ overload, increase MMP, reduce ROS levels	Activate Akt/GSK-3β pathway	[72]
	I/R-induced myocardial injury rats	Inhibit cardiomyocytes apoptosis	Decrease Bax-2/Bcl-2 ratio	[76]
	I/R-induced myocardial injury rats	Modulate energy metabolism, improve myocardial viability	Inhibit RhoA/ROCK pathway, enhance the activity and expression of mitochondrial respiratory chain complexes	[77]
	Nutritional stress-induced H9c2 cell	regulate mitochondrial autophagy and inhibite apoptosis	Activate AMPK and PINK1, dissociate of Bcl-2-Beclin1 complex	[78,82]
	H/R-induced H9c2 cells	Inhibit endoplasmic reticulum stress, reduce cardiomyocyte damage and apoptosis	Activate the PI3K/Akt signaling pathway by phosphorylating Akt	[79]
	H/R-induced H9c2 cells	Increase cellular ATP content, inhibit autophagosomal formation and apoptosis	Prevent AMPK activation, promote mTOR activation	[81]
	Myocardial I/R-induced diabetes rats	Inhibit cardiomyocytes apoptosis	Activate HIF-1α/ERK pathway, decrease Bax-2/Bcl-2 ratio, reduce caspase-3 and caspase-9 activity	[80]
	Hypoxia-induced H9c2 cells	Increase cell viability, decrease cell apoptosis and autophagy	Activate PI3K/AKT/mTOR pathway, upregulate Bcl-2 and p62, downregulate caspase-9, caspase-3, LC3-II/LC3-I, and Beclin-1	[83]
	I/R-induced myocardial injury rats	Decrease infarct size, reduce cardiomyocyte apoptosis, lower levels of TNF-α, IL-1β, and p65 protein.	Inhibit NF-κB pathway, Increase IκB expression	[85]
	LPS-induced cardiac dysfunction mice;	Suppress inflammation, restore cardiac function	Inhibit TLR4/NF-κB/NLRP3 pathway, downregulate TLR4, NF-κB, and NLRP3	[86]
	LPS-induced NRCMs
	I/R-induced rats;	Reduce IL-1β and TNF-α mRNA expression, maintain stable IL-10 expression, reduces cardiac inflammation and fibrosis	Promote macrophage M2 polarization	[87]
	BMDMs
Inhibit cardiac hypertrophy	Angiotensin II and isoproterenol-stimulated neonatal rat cardiomyocytes	Mitigate myocardial hypertrophy, downregulate ANP	Upregulate SIRT1 and PGC-1α expression	[10]
	AAC-induced cardiac hypertrophy rats	Alleviate cardiac hypertrophy, improve cardiac hemodynamic function	Inhibit TNF-α/NF-kB pathway	[90]
	AAC-induced left ventricular hypertrophy rats	Ameliorate left ventricular hypertrophy	Inhibit CaN/MAPK pathway	[91]
	ISO-induced H9c2 cells	Inhibit cardiomyocyte hypertrophy	Inhibit Ca 2+/calpain-1 pathway	[92]
	TAC-induced left ventricular hypertrophy rats	Ameliorate left ventricular hypertrophy, improve cardiac dysfunction	Regulate expression of SIRT1 and PGC-1α, activate Akt, inhibit TNF-α/NF-κB and p38 MAPK signaling pathways	[93]
Improve myocardial fibrosis	LAD ligation-induced MI mice;	Enhance cell viability, reduce apoptosis, attenuate fibrotic remodeling	Activate SIRT1/PINK1/Parkin pathway	[95]
	H2O2-induced H9C2 cells
	AAC-induced rats	Alleviate cardiac fibrosis, improve cardiac decompensation	Inhibit [Ca2+]i increase, activate the CaN/NFAT3 pathway	[97]