Bo-Ram Choi ‧ Dahye Yoon ‧ Jae-Suk Ban ‧ Woo-Cheol Shin ‧ Jin-Kyu Jang ‧ Hyeon Seon Na ‧ Dae Young Lee. JABC 2024;67:253-60. https://doi.org/10.3839/jabc.2024.035

Alcohol-induced liver damage (AILD), characterized by oxidative stress and inflammation, is a major health concern. While black ginseng extract (BGE) exhibits diverse pharmacological activities, its protective effects against AILD and underlying molecular mechanisms remain unclear. This study evaluated the protective effects of BGE against AILD using in vivo, in vitro, and in silico models. In mice, daily oral administration of 25% ethanol (5 g/kg) for 2 weeks induced liver injury. BGE (100–500 mg/kg) significantly reduced serum alanine aminotransferase (AST) and aspartate aminotransferase (ALT)levels while increasing catalase (CAT) and superoxide dismutase (SOD) activities. In ethanol-treated HepG2 cells, BGE inhibited nitric oxide (NO) production and suppressed cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) expression while increasing heme oxygenase-1 (HO-1)expression. Ginsenoside Rh1, quantified at 4.7 mg/g via quadrupole linear ion trap tandem mass spectrometry coupled with UPLC (UPLC-Q-TRAP-MS/MS), was identified as a key bioactive compound. Network pharmacology and molecular docking analyses revealed key inflammatory signaling pathways and core hub genes associated with ginsenoside Rh1. Integrated analyses suggest that ginsenoside Rh1 contributes to the multi-target effects of BGE by modulating inflammatory signaling pathways. Collectively, BGE is a potential therapeutic candidate for the prevention and treatment of AILD, with ginsenoside Rh1 serving as a key bioactive constituent and quality control marker.

Ginseng sprouts (Panax ginseng C.A. Meyer) are mostly cultivated under controlled indoor conditions, allowing modulation of growth and phytochemical composition through environmental and hormonal treatments. In this study, ¹H NMR and UPLC-QTOF/MS were used to investigate the independent and interactive effects of light intensity and gibberellic acid (GA₃) on primary metabolism and ginsenoside profiles. While GA₃ promoted shoot growth, high light reduced plant height but increased root dry weight. Multivariate analysis of 42 identified primary metabolites and 26 ginsenosides revealed that the primary metabolite profiles are primarily distinguished by GA₃, whereas ginsenoside profiles are more clearly differentiated based on light intensity. GA₃ broadly increased soluble carbohydrates and decreased free amino acids, whereas light intensity had a selective effect on some primary metabolites. In contrast to the limited interaction effects in primary metabolism, significant interactions between light and GA₃ were detected for eight ginsenosides. High-intensity light increased the content of several ginsenosides, including Re, Rg1, Rd, Rb2, and Rc, while decreasing protopanaxadiol (PPD)-type ginsenosides that lack a sophorosyl moiety at C-3. Correlation analysis across the experimental conditions revealed coordinated variation between primary metabolites and ginsenosides, with the most prominent pattern corresponding to the light-response axis. Overall, GA₃ and light intensity exerted distinct but interconnected effects across metabolic layers, providing a framework for understanding how cultivation factors determine growth and phytochemical composition in ginseng sprouts.

Bo-Ram Choi ‧ Woo-Cheol Shin ‧ Jeong Hyun Park ‧ Dahye Yoon ‧ Jin-Kyu Jang ‧ Hyeon Seon Na ‧ Yong Jae Jeong ‧ Dae Young Lee. JABC 2025;68:470-5. https://doi.org/10.3839/jabc.2025.058