Hong Jin Lee

Allergic asthma, the most common phenotype of asthma, is a chronic inflammatory airway disease driven by Type 2 immune responses and characterized by eosinophilic infiltration, elevated IgE levels, and activation of inflammatory pathways. This study investigated the anti-inflammatory and immunomodulatory effects of Perilla frutescens var. acuta Kudo extract (PFE), a plant rich in rosmarinic acid (RA), using an ovalbumin (OVA)-induced mouse model of allergic asthma. Given RA’s well-documented anti-allergic properties, extraction conditions were optimized to maximize RA yield. PFE treatment significantly reduced immune cell infiltration in bronchoalveolar lavage fluid, suppressed Th2-associated cytokine production, and decreased serum IgE levels, thereby alleviating airway inflammation. Mechanistically, PFE inhibited activation of NF-κB and p38 MAPK pathways, key drivers of inflammatory responses in allergic asthma. These findings suggest that PFE attenuates allergic airway inflammation through both immune regulation and suppression of pro-inflammatory signaling, supporting its potential as a natural therapeutic agent for allergic asthma.

In our previous study, the combination of Korean Sajabal mugwort extract (SME) and green tea extract (GTE) at a 9:1 ratio showed synergistic effects on blood flow. In this study, we evaluated the antioxidant activity of the mixture of SME and GTE, and the significance of synergy was confirmed by combination index (CI) value. SME and GTE mixture exhibited synergistic antioxidant activity, compared to individual treatments, and reduced H₂O₂-induced intracellular ROS in a dose-dependent manner. In isoproterenol (ISO)-treated animal model, oral administration of SME and GTE mixtures mitigated ISO-induced oxidative stress by enhancing antioxidant enzyme activities such as glutathione peroxidase (GPx) and glutathione reductase (GR) and activating Nrf2/Keap1 signaling. The mixture of the major components, eupatilin and jaceosidin in SME and EGCG in GTE, exerted similar synergistic antioxidant activity in vitro and in vivo. In conclusion, the SME and GTE mixture possesses a significant synergistic effect on reducing oxidative stress. Graphical abstract

In this study, we investigated the beneficial effect of solasodine, a steroidal alkaloid from Solanaceae plants, on suppressing the proliferation of gastric cancer cells by targeting Hedgehog (Hh) signaling. Solasodine inhibited the proliferation of AGS and MKN74 gastric cancer cells and regulated cell cycle (Cyclin D1 and p27) and apoptosis (Bax and Bcl-2) markers in a dose-dependent manner, consistent with the Gli1/2 inhibitor Gant61 but not the Smo inhibitor vismodegib. As an upstream regulator, solasodine inhibited Hh signaling by down-regulating Gli1 expression and blocking its nuclear localization without affecting Smo levels. Molecular docking revealed stable binding of solasodine to Gli1, with a binding affinity of −7.4 kcal/mol. Moreover, solasodine inhibited Gli1 rather than Smo expression in Hh signaling overexpressed Ptch (−/−) MEF cells. Our findings demonstrate that solasodine inhibits gastric cancer proliferation by targeting Hh/Gli1 signaling, underscoring its potential as a potent agent for prevention and/or inhibition of gastric cancer.

Garcinone C, a xanthone derived from Garcinia mangostana L , possesses antioxidant and anti-cancer effects. However, its role in gastric cancer remains unexplored. This study aimed to investigate the effects of garcinone C on gastric cancer cell proliferation and its underlying mechanism. We found that garcinone C suppressed gastric cancer cell growth by inducing G0/G1 arrest and apoptosis in a dose-dependent manner. Furthermore, garcinone C downregulated G0/G1 phase markers Cyclin D1 and p21, as well as apoptosis markers Bax, Bcl-2, cleaved-PARP, and c-caspase 3. Following the previous evidence demonstrated that aberrant Hedgehog (Hh) signaling is implicated in gastric cancer development, we confirmed that inhibiting Gli1/2 reduced the growth of AGS and MKN74 cells. Furthermore, garcinone C exerted similar effects to Gant61, inhibiting Hh signaling by reducing Gli1/2 levels and blocking their nuclear translocation. These findings suggest that garcinone C inhibits gastric cancer proliferation via the Hh signaling, indicating its potential as a therapeutic agent for treating gastric cancer.

After confirmation of Arnebia euchroma by genetic analysis, we identified the key compounds from the root: alkannin (1), acetylalkannin (2), β-acetoxyisovaleryl alkannin (3), isobutyryl alkannin (4), and β,β-dimethylacryloyl alkannin (DMA) (5). Among these, DMA most effectively inhibited the proliferation of triple-negative breast cancer (TNBC) cells, with IC₅₀ values of 5.1 μM (MDA-MB-231) and 8.7 μM (MCF10DCIS.com). DMA and the Hedgehog (Hh) inhibitor Gant61 targeting Gli1 significantly induced apoptosis, as indicated by increased Bax and cleaved PARP, and decreased Bcl-2 levels (p < 0.01) in both cell lines. We also identified AKT as a potential target of DMA, as treatment reduced phosphorylated AKT (Ser473) protein levels by 66.3% ± 0.7% and 30.1% ± 5.7% in MDA-MB-231 and MCF10DCIS.com cells, respectively (p < 0.01). In vivo, DMA (25 mg/kg) suppressed MDA-MB-231 xenograft tumor growth by approximately 78% (p < 0.01) and induced apoptosis through regulating AKT/Hh/Gli1 axis. Interestingly, the reduced form of DMA (5') lost its efficacy in inhibiting proliferation, p-AKT expression, and Gli1 transcriptional activity and nuclear localization, indicating that the Michael acceptor in DMA is critical for inhibiting TNBC growth. Overall, DMA suppressed TNBC in vitro and in vivo through AKT/Gli1 pathway and shows potential as a potent agent against TNBC.

Garcinone C, a xanthone derived from Garcinia mangostana L, possesses antioxidant and anticancer effects. However, its role in gastric cancer remains unexplored. This study aimed to investigate the effects of garcinone C on gastric cancer cell proliferation and its underlying mechanism. We found that garcinone C suppressed gastric cancer cell growth by inducing G0/G1 arrest and apoptosis in a dose‐dependent manner. Furthermore, garcinone C downregulated G0/G1 phase markers cyclin D1 and p21, as well as apoptosis markers Bax, Bcl‐2, cleaved‐PARP, and c‐caspase 3. Following the previous evidence demonstrated that aberrant Hedgehog (Hh) signaling is implicated in gastric cancer development, we confirmed that inhibiting Gli1/2 reduced the growth of AGS and MKN74 cells. Furthermore, garcinone C exerted similar effects to Gant61, inhibiting Hh signaling by reducing Gli1/2 levels and blocking their nuclear translocation. These findings suggest that garcinone C inhibits gastric cancer proliferation via the Hh signaling, indicating its potential as a therapeutic agent for treating gastric cancer.

This study aimed to evaluate the effects of Korean Sajabal mugwort extract (SME), green tea extract (GTE), and their optimized combination on improving blood flow. We first found that SME and GTE significantly suppressed TNF-α-induced ICAM-1 expression and enhanced endothelial nitric oxide synthase (eNOS) activation in EA.hy926 endothelial cells. Based on synergistic effects on regulation of IκBα, the mixture of SME and GTE at 9:1 ratio was determined as the optimal combination, and it also suppressed integrin LFA-1 expression, reducing leukocyte-endothelial cell interactions. The major components of SME (eupatilin and jaceosidin) and GTE (EGCG) were quantified, and their effects were consistent with the extracts. Furthermore, the mixture alleviated pulmonary vein occlusion, and decreased mRNA levels of ICAM-1, VCAM-1, P-selectin, and E-selectin in aortic tissue in collagen/epinephrine-induced thrombosis rat model. Taken together, the SME and GTE mixture effectively improved blow flow and may be a potent agent for preventing thrombosis and atherosclerosis.

In this study, we quantified quercetin content in onion peel extract (OPE) and investigated the effects of OPE and the equivalent amount of quercetin on lipid disorder induced by high fat diet (HDF). OPE reduced triglyceride (TG) level in oral lipid tolerance test. OPE administration improved lipid profile by lowering the level of total cholesterol (T-Chol) and LDL and by improving HDL/T-Chol ratio in HFD-fed rats. OPE also regulated hepatic expression of sterol regulatory element-binding protein 1 (SREBP-1), fatty acid synthase (FAS), peroxisome proliferator-activated receptor α (PPARα), and carnitine palmitoyltransferase-1A (CPT1A). More importantly, quercetin at the same concentration with OPE exerted similar efficacies in lipid profiles and expression of SREBP-1, FAS, PPARα, and CPT1A. Taken together, OPE possessing the key functional constituent quercetin inhibited lipid absorption and lowered serum levels of TG, cholesterol, and LDL by regulation of de novo lipogenesis and fatty acid β-oxidation, contributing to dyslipidemia improvement.

A skeletal muscle disorder has drawn attention due to the global aging issues. The loss of skeletal muscle mass has been suggested to be from the reduced muscle regeneration by dysfunction of muscle satellite cell/fibro-adipogenic progenitor cells and the muscle atrophy by dysfunction of mitochondria, ubiquitin–proteasome system, and autophagy. In this review, we highlighted the underlying mechanisms of skeletal muscle mass loss including Notch signaling, Wnt/β-catenin signaling, Hedgehog signaling, AMP-activated protein kinase (AMPK) signaling, and mammalian target of rapamycin (mTOR) signaling. In addition, we summarized accumulated studies of natural resources investigating their roles in ameliorating the loss of skeletal muscle mass and demonstrating the underlying mechanisms in vitro and in vivo. In conclusion, following the studies of natural resources exerting the preventive activity in muscle mass loss, the signaling-based approaches may accelerate the development of functional foods for sarcopenia prevention.