Biology subjects

Han, B.-C.

Publications and source records attributed to Han, B.-C..

3 recordsLinked to original sources

bioRxiv2025

G1899, an American ginseng extract, alleviates neuroinflammation and cognitive impairment in models of Alzheimer's disease

BackgroundAlzheimers disease (AD) is characterized by amyloid {beta} (A{beta}) accumulation, tau pathology, and chronic neuroinflammation, yet current therapeutic strategies provide only limited efficacy. Natural compounds with pleiotropic actions have emerged as potential adjunctive interventions. This study evaluated G1899, a standardized American ginseng (Panax quinquefolius) extract, for its effects on neuroinflammation, A{beta} clearance, and cognitive function. MethodsNeuronal cultures were exposed to glutamate or A{beta} oligomers (A{beta}o) and pre-treated with G1899 to assess cell viability and excitotoxicity. Primary murine microglia were analyzed for validating expression levels of TMEM119, CD68, NLRP3 inflammasome, IL-1{beta}, Caspase-1, and STAT3 phosphorylation. Behavioral testing was performed in scopolamine-injected mice with short term G1899 treatment and in 5xFAD transgenic mice following long-term G1899 administration at multiple doses. Amyloid burden, microglial recruitment, and plaque morphology were quantified by immunohistochemistry and high-resolution imaging. Human induced microglia (iMG) were examined for neuroinflammatory responses following A{beta}o exposure with or without G1899 treatment. ResultsG1899 significantly improved neuronal viability and reduced glutamate- and A{beta}o-induced toxicity. In microglia, G1899 upregulated TMEM119 and CD68, while suppressing NLRP3 inflammasome formation, proinflammatory cytokine expression, and STAT3 phosphorylation. G1899 rescued scopolamine-induced memory deficits and, in 5xFAD mice, reduced hippocampal and cortical A{beta} burden, alleviated neuroinflammatory markers, and improved both spatial/fear learning and memory, with the most consistent efficacy observed at 300 mg/kg. Imaging revealed enhanced microglial recruitment to plaques and facilitated fragmentation of A{beta} deposits. In iMG, G1899 elevated homeostatic and phagocytic markers while attenuating A{beta}o-induced NLRP3/STAT3-mediated neuroinflammatory signaling pathway. ConclusionsG1899 confers multimodal neuroprotection by preserving neuronal survival, modulating microglial activity, and facilitating A{beta} clearance. These findings highlight its potential as a safe and clinically translatable botanical intervention for AD.

neuroscience↗

bioRxiv2025

American ginseng (Panax quinquefolius L.) extracts (G1899) reverse stress-induced behavioral abnormalities in mice

Stress affects brain functions, which leads to the development of mental disorders like anxiety, depression, cognitive decline, and social dysfunction. There is increasing focus on the role of nutritional, herbal and nutraceutical compounds on mental and cognitive functioning. Interestingly, studies suggest that American ginseng (Panax quinquefolius L.) extracts (G1899) improve cognition. We thus examined whether G1899 showed protective effects on stress-induced behavioral changes in animals. 200 mg/kg G1899 was orally administered daily for 4 weeks to 2-3-month-old female and male mice before inducing stress. To induce acute stress in animals, we intraperitoneally injected a low dose of lipopolysaccharides (LPS) (10 g/kg), and saline was used as a control. We also used chronic restraint stress (CRS) as a chronic stress model in mice. After LPS injection or CRS, multiple behavioral assays were carried out - a sucrose preference test, an open filed test, reciprocal social interaction, contextual fear conditioning, and a tail suspension test - to determine whether acute or chronic stress affected animals behaviors and whether G1899 had protective effects against stress-induced behavioral dysfunction. We found that both LPS injection and CRS induced stress-related behavioral dysfunction, including depression-like behavior, anhedonia, social dysfunction, and fear memory impairments in both females and males. However, G1899 treatment was sufficient to reverse stress-induced behavioral abnormalities in animals. Our data further suggested that G1899 reduced the activity of hippocampal neurons by suppressing glutamatergic activity. Our study suggests that G1899 supplements can be protective against both acute and chronic stress in mice by suppressing neuronal and synaptic activity. HighlightsO_LIAmerican ginseng (Panax quinquefolius L.) extract (G1899) treatment reverses acute stress-induced behavioral dysfunction in mice. C_LIO_LIG1899 treatment reverses chronic stress-induced behavioral dysfunction in mice. C_LIO_LIG1899 treatment reduces serum corticosterone levels in chronically stressed mice. C_LIO_LIG1899 treatment suppresses glutamatergic activity in hippocampal neurons. C_LI

neuroscience↗

bioRxiv2024

Downregulation of O-GlcNAcylation enhances etoposide-induced p53-mediated apoptosis in HepG2 human liver cancer cells

Etoposide, an anticancer drug that inhibits topoisomerase II, is commonly used in combination chemotherapy. However, the impact of O-GlcNAcylation regulation on etoposides anticancer effects has rarely been investigated. This study evaluated the effect of etoposide on cellular O-GlcNAcylation and whether modulating this process enhances etoposide-induced apoptosis. O-GlcNAc expression was measured after 24 h of etoposide treatment, and the effect of O-GlcNAc transferase (OGT) inhibition by OSMI-1 on etoposides anticancer activity in HepG2 human liver cancer cells was quantitatively analyzed. Additionally, molecular analyses were used to confirm that the observed effects were mediated by p53-induced apoptosis. Etoposide reduced O-GlcNAcylation in a dose-dependent manner without directly interacting with OGT. Cotreatment with 20 M of OSMI-1 lowered the IC50 value for cell viability by approximately 1.64-fold to 60.68 M and increased the EC50 value for cytotoxicity by around 4.07-fold to 43.41 M. Furthermore, this synergistic effect was linked to the activation of the p53/caspase-3/PARP1 pathway. These findings suggest that downregulating O-GlcNAcylation may enhance the efficacy of etoposide-based chemotherapy and help overcome tumor resistance. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/626030v2_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@3cb205org.highwire.dtl.DTLVardef@cb686forg.highwire.dtl.DTLVardef@356662org.highwire.dtl.DTLVardef@1d4dc40_HPS_FORMAT_FIGEXP M_FIG Etoposide, a topoisomerase II inhibitor, reduces O-GlcNAcylation in HepG2 liver cancer cells. Further inhibition of O-GlcNAc transferase by OSMI-1 enhanced etoposide-induced apoptosis, lowering the IC50 for viability and increasing the EC50 for cytotoxicity. This synergy was mediated by the p53, caspase-3/7, PARP1 pathway, suggesting that targeting O-GlcNAcylation may improve etoposide efficacy. C_FIG

molecular biology↗