Hao Yue

Isoprenaline (ISO) can cause chronic heart failure (CHF) by inducing cardiomyocyte apoptosis and oxidative stress. Polysaccharides present in Panax ginseng C. A. Mey. (Ginseng) exhibit potent antioxidant and anti-apoptotic properties, improve hypoxic conditions within the body, and mitigate the damage caused by oxidative stress. This study investigated the activity of ginseng polysaccharides (GP) from different harvest years and their mechanisms of action in alleviating CHF by using in vivo and in vitro experimental validation. In this study, 5-year-old GP (5y-GP) and 15-year-old GP (15y-GP) were obtained via water extraction and alcohol precipitation. Their protective effects against ISO-induced damage in the H9c2 cell line and antioxidant activities were evaluated. Among these, 15y-GP demonstrated strong biological activity. Subsequently, four fractions were eluted from 15y-GP using a DEAE-52 column and the four polysaccharide components were evaluated; of these, component 15y-GP4 exhibited the strongest biological activity. 15y-GP4 was characterized by Fourier-transform infrared and monosaccharide composition analysis, and its preventive effects on ISO-induced CHF were investigated. 15y-GP4 was characterized as an acidic heteropolysaccharide with high glucuronic acid content. It effectively reduced levels of reactive oxygen species, improved mitochondrial function in myocardial cells, and inhibited apoptosis. Furthermore, 15y-GP4 alleviated ISO-induced CHF by downregulating PI3K/AKT/hypoxia-inducible factor-1α (HIF-1α) expression, while upregulating phosphatase 6 regulatory subunit 2 (SAPS2) and protein phosphatase 6 (PP6) catalytic subunit (PPP6C) expression. Immunoprecipitation and co-localization techniques revealed an association between HIF-1α and PP6, with both playing crucial roles in CHF. These results indicate that 15y-GP4 possesses superior bioactivity in preventing CHF, demonstrating broad prospects for the development of CHF applications.

American ginseng ( Panax quinquefolium L.) is a traditional Chinese medicinal herb that has been used in China for hundreds of years. The significant hypoglycemic activity of American ginseng has made it widely used in health food as a valuable medicinal herb with homologous origin. However, its effect and mechanism of improving insulin resistance (IR) remain unclear. In the present study, an IR‐HepG2 cells model induced by high concentrations of insulin was constructed and treated with ethanol extract of dried American ginseng (EDAG) at different concentrations to reveal the in vitro ameliorative effect of EDAG on IR by monitoring glucose consumption, glycogen content, triglyceride (TG) content, and total cholesterol (TC) content of the cells. The cell metabolite changes were tracked by liquid chromatography‐mass spectrometry (LC‐MS)‐based metabolomics combined with multivariate statistical analysis, the metabolic biomarkers and related metabolic pathways were analyzed, and further elucidate its mechanism of action. The results showed that treatment with EDAG increased glucose consumption and glycogen content, and decreased intracellular TC and TG content in IR‐HepG2 cells to different degrees. The results of cell metabolomics indicated that EDAG treatment reversed metabolic disorders by regulating sphingolipid metabolism, linoleic acid metabolism, and arginine and proline metabolism, etc. The present study explored the in vitro IR improvement mechanism of EDAG based on the LC‐MS cell metabolomics approach, which confirms the great potential of LC‐MS technology in the evaluation of drug efficacy and can be an effective tool for the related analysis of other Chinese herbal medicines.

Ginseng is a Chinese medicine known for its tonic effect. Numerous studies have shown that ginseng exerts therapeutic effects on cancer cells. Hypoxia-inducible factor-1α (HIF-1α) is an important transcriptional regulator in response to a hypoxic environment and is crucial in the adaptation of tumor cells to the hypoxic environment. During tumor growth, HIF-1α regulates the activity of various transcription factors and their downstream molecules by modulating various biological processes, including cell proliferation, growth, angiogenesis, and metastasis. Therefore, high HIF-1α expression may be closely associated with poor prognosis in patients with various solid tumors. Pharmacological targeting of HIF-1α is considered a therapeutic strategy for cancer treatment. To investigate the molecular mechanism of ginseng’s effect on cancer through HIF-1α, a more detailed and in-depth analysis is needed. In this review, we present ginseng as a HIF-1α inhibitor that can inhibit tumor development in vivo and in vitro cancer models. These results may clarify the relationship between HIF-1α and ginseng in cancer treatment.

This study aimed to investigate the anti-aging properties and underlying mechanisms of Nitraria anthocyanin (NA) and wild ginseng saponin (WG) in HaCaT cells. Ultra-performance liquid chromatography Q Exactive high-resolution mass spectrometry and ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry were used to analyze WG and NA, and HaCaT cells were subjected to treatment with WG and NA, followed by assessment of cell viability, expression levels of extracellular matrix components, and analysis of the mitogen-activated protein kinase signaling pathway. We identified 36 ginsenoside components in WG and 7 anthocyanin components in NA, which corresponded to 4 types: cyanidin, malvidin, delphinidin, and pelargonin. 80 μg/mL NA and 4 μg/mL WG (NAWG-3) significantly promoted cell proliferation and energy metabolism in HaCaT cells, while also enhancing the cellular hyaluronic acid content and elevating the expression levels of collagen I, elastin, and components of the mitogen-activated protein kinase pathway. Furthermore, WG and NA downregulate the mRNA expression of matrix hydrolases. The anti-aging effects of NAWG-3 on the skin were achieved through the stimulation of HaCaT cell activity, promotion of extracellular matrix component expression, and inhibition of their degradation.

Background: Abnormal activation of Angiotensin II (Ang II) serves as a primary trigger for myocardial hypertrophy and cardiac injury. Isoquercitrin (IQ) and Quercetin (Que) possess anti-inflammatory and anti-apoptotic properties, but their protective effects against Ang II-induced cardiac injury remain unclear. This study aimed to investigate the mechanisms and therapeutic efficacy of IQ and Que in heart failure. Methods: Cytotoxic effects of IQ and Que on Ang II-induced H9c2 rat cardiomyocyte apoptosis models were assessed in vitro using the CCK-8 assay. Reactive Oxygen Species (ROS) generation and apoptotic fluorescence levels were measured. WB analysis examined protein expression in inflammatory and apoptotic pathways. In vivo heart failure model was established in mice, with cardioprotective effects of IQ and Que evaluated via echocardiography. Molecular docking was employed to analyze ligand–target interactions. Results: IQ outperformed Que in promoting cell viability and decreasing ROS. IQ exhibited a more potent inhibitory effect on apoptosis through regulating Bax, Caspase-3, CytoC, and Bcl-2 and demonstrated superior suppression of cardiac inflammation by inhibiting phosphorylation of ERK, JNK, and P38. Compared with Que, IQ more effectively attenuated Ang II-induced cardiac injury by ameliorating reductions in EF% and FS%, suppressing ST-segment elevation, and significantly reducing serum levels of CK-MB, LDH, ANP, BNP, and FFA in a heart failure model. Molecular docking verified stronger binding affinity of IQ for key targets. Conclusions: IQ demonstrates superior cardioprotection over Que by regulating MAPK signaling and mitochondrial apoptosis pathways, supporting its potential as a therapeutic candidate for heart failure.

Tao Ren, Dihao Li, Feng Sun, Lijia Pan, Ao Wang, Xinze Li, Yuwen Bao, Meiyu Zhang, Fei Zheng, and Hao Yue. J. Microbiol. Biotechnol. 2025;35:1-13. https://doi.org/10.4014/jmb.2503.03045