👤 Jeong-Hui Je

The potential anti-obesity, anti-inflammatory, and anti-oxidative stress properties of ark shell-derived LLRLTDL (Bu1) and GYALPCDCL (Bu2) peptides were comprehensively investigated. In bone marrow-derived mesenchymal stem cells (BMMSCs), both peptides demonstrated significant anti-adipogenic effects by downregulating key adipogenic transcription factors, including peroxisome proliferator-activated receptor gamma (PPAR-γ), CCAAT/enhancer-binding protein alpha (C/EBPα), and sterol regulatory element-binding protein 1 (SREBP-1) and their downstream adipocyte-specific genes including adipocyte fatty acid-binding protein 2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL). Mechanistically, Bu1 and Bu2 promoted lipolysis through the activation of AMP-activated protein kinase (AMPK) and hormone-sensitive lipase (HSL). These peptides also exhibited potent anti-oxidative stress activity by suppressing reactive oxygen species generation and activating the HO-1/Nrf2 signaling pathway, as confirmed through HO-1 siRNA silencing. In addition, Bu1 and Bu2 demonstrated robust anti-inflammatory effects by reducing pro-inflammatory cytokine production and inhibiting MAPK signaling pathways. These findings were corroborated in a high-fat diet (HFD)-induced mouse model, where oral administration of Bu1 and Bu2 resulted in significant reductions in body weight, weight gain, and adipose tissue accumulation, along with decreased expression of adipogenic transcription factors and genes while improving serum cholesterol levels, and exhibited anti-oxidative stress effects via HO-1/Nrf2 activation. Collectively, these results underline the potential of Bu1 and Bu2 as multi-target therapeutic agents against obesity and related metabolic disorders. Show less

SH003, a novel herbal mixture consisting of NSCLC cell lines (A549, H460, HCC827) were treated with SH003 to evaluate cell viability (MTT assay), colony formation, apoptosis (Annexin V/7-AAD staining, western blot), and cell cycle distribution (PI staining). Phosphorylation of RTKs and related signaling molecules was analyzed using a phospho-RTK array and western blot. NSCLC cell lines A549, H460, and HCC827 treated with SH003 showed significant, dose-dependent cell viability and colony formation reductions. SH003 induced apoptosis, evidenced by increased cleaved PARP and caspase-8 levels, and caused G SH003 is a promising multi-target therapeutic agent for NSCLC, offering a novel strategy to improve patient outcomes. Show less

Collaborative regulation of liver X receptor (LXR) and sterol regulatory element binding protein (SREBP)-1 are main determinants in hepatic steatosis, as shown in both animal models and human patients. Recent studies indicate that selective intervention of overly functional LXRα in the liver shows promise in treatment of fatty liver disease. In the present study, we evaluated the effects of meso-dihydroguaiaretic acid (MDGA) on LXRα activation and its ability to attenuate fatty liver in mice. MDGA inhibited activation of the LXRα ligand-binding domain by competitively binding to the pocket for agonist T0901317 and decreased the luciferase activity in LXRE-tk-Luc-transfected cells. MDGA significantly attenuated hepatic neutral lipid accumulation in T0901317- and high fat diet (HFD)-induced fatty liver. The effect of MDGA was so potent that treatment with 1mg/kg for 2 weeks completely reversed the lipid accumulation induced by HFD feeding. MDGA reduced the expression of LXRα co-activator protein RIP140 and LXRα target gene products associated with lipogenesis in HFD-fed mice. These results demonstrate that MDGA has the potential to attenuate nonalcoholic steatosis mediated by selective inhibition of LXRα in the liver in mice. Show less