Effect of Sopoongsan on Skin Inflammation and Hyperlocomotion in Socially Isolated Mice with Atopic Dermatitis.

Psychological stress is a major exacerbating factor of atopic dermatitis (AD), a chronic inflammatory skin disease. Sopoongsan (SPS), a traditional herbal formula, has been indicated for the treatment of various skin disorders, including AD. This study investigated the effects of SPS on a 2,4-dinitrochlorobenzene- (DNCB-) induced AD mice model exposed to social isolation (SI) stress. The severity of the AD symptoms and behavioral abnormalities was evaluated. SPS reduced the clinical skin score as evaluated with the SCORing Atopic Dermatitis (SCORAD) index and suppressed the cutaneous infiltration of T-lymphocyte cells, mast cells, and eosinophils in SI-AD mice. The SPS treatment decreased the total distance and mean speed and increased resting time in the open field test (OFT) for these mice. In addition, the time spent in the social zone in the social interaction test also improved when SPS treatment was given. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the prefrontal cortex (PFC) in the SI-AD mice were reduced by the oral administration of SPS. HaCaT and BV2 cells were used for the in vitro experiments. The pretreatment with SPS reduced the protein levels of the thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC) in the HaCaT cells stimulated with TNF-α and interferon-gamma (IFN-γ) (TI). SPS also suppressed TNF-α and IL-6 secretion in lipopolysaccharide- (LPS-) stimulated BV2 cells. These results imply that SPS could be a promising candidate for the treatment of AD in patients under stress conditions and at risk of exacerbation.

MBP-11901 Inhibits Tumor Growth of Hepatocellular Carcinoma through Multitargeted Inhibition of Receptor Tyrosine Kinases.

Hepatocellular carcinomas (HCCs) are aggressive tumors with a poor prognosis. Approved first-line treatments include sorafenib, lenvatinib, and a combination of atezolizumab and bevacizumab; however, they do not cure HCC. We investigated MBP-11901 as a drug candidate for HCC. Cell proliferation and cytotoxicity were evaluated using normal and cancer human liver cell lines, while Western blotting and flow cytometry evaluated apoptosis. The anticancer effect of MBP-11901 was verified in vitro through migration, invasion, colony formation, and JC-1 MMP assays. In mouse models, the tumor volume, tumor weight, and bodyweight were measured, and cancer cell proliferation and apoptosis were analyzed. The toxicity of MBP-11901 was investigated through GOT/GPT and histological analyses in the liver and kidney. The signaling mechanism of MBP-11901 was investigated through kinase assays, phosphorylation analysis, and in silico docking simulations. Results. MBP-11901 was effective against various human HCC cell lines, leading to the disappearance of most tumors when administered orally in animal models. This effect was dose-dependent, with no differences in efficacy according to administration intervals. MBP-11901 induced anticancer effects by targeting the signaling mechanisms of FLT3, VEGFR2, c-KIT, and PDGFRß. MBP-11901 is suggested as a novel therapeutic agent for the treatment of advanced or unresectable liver cancer.