Ginsenoside Rh2

Ginsenoside Rh2 (Rh2), an important phytochemical derived from Panax ginseng, has demonstrated anticancer activity, amelioration of ischemic brain injury, and mitigation of doxorubicin-induced cardiac damage. The cardioprotective effects of Rh2 were evaluated in a mouse model of acute myocardial infarction (AMI). Mice received Rh2 treatment for 14 days postsurgery, and the cardiac function was assessed by echocardiography. Rh2 treatment significantly improved left ventricular function, reduced infarct size, and suppressed cardiac fibrosis in the MI model. Furthermore, it promoted angiogenesis in the border zone, enhanced mitochondrial membrane potential and ATP production, and reduced hypoxia-induced ROS accumulation, excessive mitochondrial fission, and cardiomyocyte apoptosis. In vitro, Rh2 enhanced human umbilical vein endothelial cell (HUVEC) migration in wound-healing assays, an effect associated with an increased level of ERK phosphorylation. These effects were abolished by U0126, an ERK inhibitor. In conclusion, Rh2 protects against MI-induced cardiac injury by improving mitochondrial bioenergetics and activating an ERK-dependent pathway.

Ginsenosides, the primary bioactive constituents of ginseng, are recognized for its potential to mitigate cognitive deficits associated with neurodegenerative conditions. Nevertheless, its molecular targets within cerebral tissues remain to be elucidated. First, cellular thermal shift assay (CETSA) combined with liquid chromatography mass spectrometry (LC-MS) was used to identify potential proteins of ginsenosides intersecting in the disease databases. Secondly, biolayer interferometry (BLI) was used to detect and verify the strongest binding compounds and to predict binding sites through molecular docking. Next, the functional characteristics and molecular properties of these candidate proteins were analyzed by bioinformatics. Finally, the mRNA expression levels of candidate genes in murine hippocampus were quantified via qRT-PCR following PPD treatment. Integration of CETSA proteomic data with the disease database identified three overlapping gens. BLI analysis and molecular docking showed that compound K (CK) and ginsenoside Rh2 were well combined with postsynaptic density protein 95 (PSD95). CK and PPD work well with ATXN10. PPD, Rh2 and ANXA2 are well combined. Bioinformatics analysis suggested that the target genes were significantly enriched in AMPA glutamate receptors. qRT-PCR analysis revealed that PPD administration modulated the mRNA expression of synaptic proteins, including PSD95, ANXA2, and the AMPA receptor subunit GluA1, in murine hippocampal tissue. These results suggest that PSD95, ANXA2 and ATXN10 are potential brain targets of ginsenosides in cognitive impairment. PPD has a good effect on the mRNA expression of PSD95, ANXA2 and GluA1 in the brain of mice with cognitive impairment.