Dae Sik Jang’s research while affiliated with Kyung Hee University and other places

Background Huntington disease (HD), a neurodegenerative autosomal dominant disorder, is characterized by involuntary choreatic movements with cognitive and behavioral disturbances. Up to now, no therapeutic strategies are available to completely ameliorate the progression of HD. Schisandra chinensis has various pharmacologic effects such as antioxidant and anti-inflammatory activities. However, the neuroprotective value of seed oil of S. chinensis (SOSC) has not been elucidated yet. The purpose of this study was to determine neuroprotective effects of SOSC by supercritical fluid extraction against 3-nitropropionic acid (3-NPA)-induced HD-like symptoms and neuropathology in an experimental mouse model. Methods SOSC (75, 150, and 300 mg/kg/day) was orally pre-administration once daily at 1 hour before 3-NPA intoxication. Results SOSC ameliorated movement dysfunction and lethality following 3-NPA intoxication in connection with reduction of lesion area, neurodegeneration/apoptosis, microglial migration/activation, and mRNA expression of pro-inflammatory cytokines/enzymes in the striatum. SOSC inhibited the activation of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPKs) pathways but stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) in the striatum after 3-NPA intoxication. Schizandrin, a main component of SOSC, reduced protein expression levels of Iba-1 and p-NF-κB in 3-NPA-induced BV2 cells (murine microglia cell line). BV2 cell’s conditioned medium inhibited cleaved caspase-3 in 3-NPA-induced SH-SY5Y cells (a neuroblastoma cell line). Conclusion SOSC might ameliorate movement dysfunction by inhibiting neuropathology through its anti-inflammatory and antioxidant activities in the striata of 3-NPA-intoxicated mice. These findings suggest that SOSC could serve as a promising therapeutic candidate for HD-like symptoms, providing a foundation for future treatment strategies targeting neuroinflammation and oxidative stress.

Parkinson’s disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons. In particular, neuroinflammation associated with phosphorylation of c-Jun N-terminal kinase (JNK) is likely to cause the death of dopaminergic neurons. Therefore, protecting dopaminergic neurons through anti-neuroinflammation is a promising therapeutic strategy for PD. This study investigated whether Tribuli Fructus (TF) could alleviate PD by inhibiting neuroinflammation. Mouse primary mixed glial culture cells from the mouse cortex were treated with lipopolysaccharide (LPS) to induce neuroinflammation, and 1 h later, cells were treated with TF. 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP) was injected into C57BL/6J mice for 5 days, and TF was co and post-administered for 12 days. Our study showed that TF attenuated pro-inflammatory mediators and cytokines in LPS-stimulated primary mixed glial cultures. In the brains of MPTP-induced PD mouse model, TF inhibited the activation of microglia and astrocytes, protected dopaminergic neurons, and increased dopamine levels. TF alleviated MPTP-induced bradykinesia, a representative behavioral disorder in PD. In addition, the results in vitro and in vivo revealed that TF regulates the phosphorylation of JNK. Collectively, our data suggest that TF may be a new therapeutic candidate for PD by regulating JNK signaling.

Panax ginseng (Korean ginseng) is renowned for its health-promoting properties, attributed to its bioactive compounds, including saponins, polyphenols, and polysaccharides, which possess both antioxidant and anti-aging activities. This study investigated the anti-aging and anti-inflammatory effects of compounds isolated from the hot water extract of fresh P. ginseng roots, evaluating their resistance to TNF-α/IFN-γ-induced skin cell damage. Among 14 compounds, ginsenoside Rf (compound 2) showed significant multi-target effects. In NHDFs, ginsenoside Rf and others effectively reduced intracellular ROS, demonstrating strong antioxidant properties. Additionally, they inhibited MMP-1 expression, a key enzyme in collagen degradation, and promoted pro-collagen Type I synthesis, countering the negative effects of TNF-α and supporting skin health. Further analysis showed that ginsenoside Rf reduced the secretion of inflammatory cytokines like IL-1β and IL-6, exhibiting anti-inflammatory effects. It also promoted the expression of crucial skin barrier proteins, including LOR, AQP3, FLG, and KRT1 in TNF-α/IFN-γ-stimulated NHEKs, enhancing skin hydration and structural integrity. These results suggest that compounds from P. ginseng roots, especially ginsenoside Rf, hold promise as skincare agents targeting skin aging and inflammation. Future research should further explore their mechanisms and optimize their applications in dermatological treatments.

Atopic dermatitis is an inflammatory dermatological disease characterized by persistent scratching and recurrent eczema. Due to the influence of environmental variables on the cause of this disease, there remains an ongoing interest in the development of therapeutic interventions. Previous studies have shown that various plants of the genus Aster and its derived phytochemicals possess efficacy in treating inflammatory-mediated diseases, including atopic dermatitis. Therefore, the present study investigated a potential compound with anti-atopic dermatitis properties derived from Aster koraiensis leaves, specifically targeting HaCaT keratinocyte cells. First, we isolated eleven compounds with three unknown compounds, including two polyacetylenes (1 and 3) and a benzoic acid derivative (4). The chemical structures of the isolates were elucidated by 1D and 2D NMR, specific rotation, acid hydrolysis, and quantum chemical calculations. Next, we treated an A. koraiensis extract and all isolates to HaCaT keratinocyte, followed by stimulation with TNF-α/IFN-γ. Among bioactive compounds, astersaponin J (7) exhibited a significant reduction in the levels of inflammatory cytokines associated with atopic dermatitis at a concentration of 2.5 μM. These findings suggest that chemicals obtained from an A. koraiensis 95% ethanol extract and derived compounds are potential therapeutics to help reduce the immunological response driven by atopic dermatitis.

Asthma is a chronic inflammatory disorder of the lungs that results in airway inflammation and narrowing. BS012 is an herbal remedy containing Asarum sieboldii, Platycodon grandiflorum, and Cinnamomum cassia extracts. To elucidate the anti-asthma effect of BS012, this study analyzed the immune response, respiratory protection, and changes in metabolic mechanisms in an ovalbumin-induced allergic asthma mouse model. Female BALB/c mice were exposed to ovalbumin to induce allergic asthma. Bronchoalveolar lavage fluid and plasma were analyzed for interleukin and immunoglobulin E levels. Histological analyses of the lungs were performed to measure morphological changes. Apoptosis-related mediators were assayed by western blotting. Plasma and lung tissue metabolomic analyses were performed to investigate the metabolic changes. A T-helper-2-like differentiated cell model was used to identify the active components of BS012. BS012 treatment improved inflammatory cell infiltration, mucus production, and goblet cell hyperplasia in lung tissues. BS012 also significantly downregulated ovalbumin-specific immunoglobulin E in plasma and T-helper-2-specific cytokines, interleukin-4 and -5, in bronchoalveolar lavage fluid. The lungs of ovalbumin-inhaled mice exhibited nerve growth factor-mediated apoptotic protein expression, which was significantly attenuated by BS012 treatment. Ovalbumin-induced abnormalities in amino acid and lipid metabolism were improved by BS012 in correlation with its anti-inflammatory properties and normalization of energy metabolism. Additionally, the differentiated cell model revealed that N-isobutyl-dodecatetraenamide is an active component that contributes to the anti-allergic properties of BS012. The current findings demonstrate the anti-allergic and respiratory protective functions of BS012 against allergic asthma, which can be considered a therapeutic candidate.

This present study investigated the anti-skin-aging properties of Rosa rugosa. Initially, phenolic compounds were isolated from a hot water extract of Rosa rugosa’s flower buds. Through repeated chromatography (column chromatography, MPLC, and prep HPLC), we identified nine phenolic compounds (1–9), including a previously undescribed depside, rosarugoside D (1). The chemical structure of 1 was elucidated via NMR, HR-MS, UV, and hydrolysis. Next, in order to identify bioactive compounds that are effective against TNF-α-induced NHDF cells, we measured intracellular ROS production in samples treated with each of the isolated compounds (1–9). All isolates reduced the level of ROS at a concentration of 10 μM. Particularly, two depsides—rosarugosides A and D (2 and 1)—significantly inhibited ROS expression in TNF-α-induced NHDFs compared to the other phenolic compounds. Subsequently, the production of MMP-1 and procollagen type Ι α1 by these two depsides was examined. Remarkably, rosarugoside A (2) significantly decreased MMP-1 secretion at all concentrations. In contrast, rosarugoside D (1) regulated the expression of procollagen type Ι α1. These findings collectively suggest that Rosa rugosa extracts and their isolated compounds, rosarugosides A (2) and D (1), hold significant potential for protecting against aging and skin damage. Overall, these findings suggest that Rosa rugosa extracts and their isolated compounds, rosarugosides A (2) and D (1), have the potential to prevent and protect against aging and skin damage, although more specific quantitative analysis is needed.