Herbal extract THI improves metabolic abnormality in mice fed a high-fat diet

Target herbal ingredient (THI) is an extract made from two herbs, Scutellariae Radix and Platycodi Radix. It has been developed as a treatment for metabolic diseases such as hyperlipidemia, atherosclerosis, and hypertension. One component of these two herbs has been reported to have anti-inflammatory, anti-hyperlipidemic, and anti-obesity activities. However, there have been no reports about the effects of the mixed extract of these two herbs on metabolic diseases. In this study, we investigated the metabolic effects of THI using a diet-induced obesity (DIO) mouse model. High-fat diet (HFD) mice were orally administered daily with 250 mg/kg of THI. After 10 weeks of treatment, the THI-administered HFD mice showed reduction of body weights and epididymal white adipose tissue weights as well as improved glucose tolerance. In addition, the level of total cholesterol in the serum was markedly reduced. To elucidate the molecular mechanism of the metabolic effects of THI in vitro, 3T3-L1 cells were treated with THI, after which the mRNA levels of adipogenic transcription factors, including C/EBPα and PPARγ, were measured. The results show that the expression of these two transcription factors was down regulated by THI in a dose-dependent manner. We also examined the combinatorial effects of THI and swimming exercise on metabolic status. THI administration simultaneously accompanied by swimming exercise had a synergistic effect on serum cholesterol levels. These findings suggest that THI could be developed as a supplement for improving metabolic status

Korean Red Ginseng Enhances Immunotherapeutic Effects of NK Cells via Eosinophils in Metastatic Liver Cancer Model

Metastasis decreases the survival rate of patients with liver cancer. Therefore, novel anti-metastatic strategies are needed. Korean Red Ginseng (KRG) is often ingested as a functional food with an immune-boosting effect. We investigated a combination of KRG and natural killer (NK) cells as a novel immunotherapy approach. SK-Hep1 cells were injected into the tail vein of NRGA mice to establish an experimental metastasis model. KRG, NK cells, or a combination of KRG and NK cells were administered. Tumor growth was observed using an in vivo imaging system, and metastatic lesions were evaluated by histological analysis and immunohistochemistry. Bioluminescence intensity was lower in the KRG and NK cell combination group than in the other groups, indicating that the combination treatment suppressed the progression of metastasis. CD56 expression was used as a NK cell marker and hematological analysis was performed. The combination treatment also decreased the expression of matrix metalloproteinases and the area of metastatic lesions in liver and bone tissues, as well as increased the eosinophil count. Expression of cytokines-related eosinophils and NK cells was determined by Western blotting analysis. The expression of interleukin 33 (IL33) was induced by the combination of KRG and NK cells. High IL33 expression was associated with prolonged overall survival in the Kaplan–Meier plotter. Our results suggest that KRG enhances the immune activity of NK cells by IL-33 through eosinophils and suppresses metastatic liver cancer progression

Monofacet-Selective Cavitation within Solid-State Silica-Nanoconfinement toward Janus Iron Oxide Nanocube

Here, a highly selective solid-state nanocrystal conversion strategy is developed toward concave iron oxide (Fe3O4) nanocube with an open-mouthed cavity engraved exclusively on a single face. The strategy is based on a novel heat-induced nanospace-confined domino-type migration of Fe2+ ions from the SiO2-Fe3O4 interface toward the surrounding silica shell and concomitant self-limiting nanoscale phase-transition to the Fe-silicate form. Equipped with the chemically unique cavity, the produced Janus-type concave iron oxide nanocube was further functionalized with controllable density of catalytic Pt-nanocrystals exclusively on concave sites and utilized as a highly diffusive catalytic Janus nanoswimmer for the efficient degradation of pollutant-dyes in water

Suppression of Adipocyte Differentiation by Foenumoside B from Lysimachia foenum-graecum Is Mediated by PPARγ Antagonism.

Lysimachia foenum-graecum extract (LFE) and its active component foenumoside B (FSB) have been shown to inhibit adipocyte differentiation, but their mechanisms were poorly defined. Here, we investigated the molecular mechanisms responsible for their anti-adipogenic effects. Both LFE and FSB inhibited the differentiation of 3T3-L1 preadipocytes induced by peroxisome proliferator-activated receptor-γ (PPARγ) agonists, accompanied by reductions in the expressions of the lipogenic genes aP2, CD36, and FAS. Moreover, LFE and FSB inhibited PPARγ transactivation activity with IC50s of 22.5 μg/ml and 7.63 μg/ml, respectively, and showed selectivity against PPARα and PPARδ. Rosiglitazone-induced interaction between PPARγ ligand binding domain (LBD) and coactivator SRC-1 was blocked by LFE or FSB, whereas reduced NCoR-1 binding to PPARγ by rosiglitazone was reversed in the presence of LFE or FSB. In vivo administration of LFE into either ob/ob mice or KKAy mice reduced body weights, and levels of PPARγ and C/EBPα in fat tissues. Furthermore, insulin resistance was ameliorated by LFE treatment, with reduced adipose tissue inflammation and hepatic steatosis. Thus, LFE and FSB were found to act as PPARγ antagonists that improve insulin sensitivity and metabolic profiles. We propose that LFE and its active component FSB offer a new therapeutic strategy for metabolic disorders including obesity and insulin resistance

In vivo effects of LFE on ob/ob mice.

<p>LFE (100 or 300 mg/kg; n = 10 per group) was orally administered once daily for 8 weeks to 6-week-old ob/ob mice. Body weights (A left), food intakes (A right), and plasma glucose levels (B) were measured weekly. After 8 weeks of treatment, OGTT (C) and ITT (D) were carried out. Fasting plasma glucose levels after 8 weeks treatment were measured (E). Experiments were repeated twice, and results are presented as means ± SDs. *P<0.05, **P<0.01 vs. vehicle (0.05% CMC).</p

Effects of LFE on hepatic steatosis in ob/ob mice.

<p>After 8 weeks of LFE administration, plasma levels of ALT and AST, and TG were determined using commercial kits (A). Liver tissues were frozen and tissue sections were stained with either H&E or Oil Red O, and visualized under an optical microscope (B). Hepatic TG contents were measured using commercial kit (C). Plasma levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) were measured using ELISA kits (D). Hepatic mRNA levels of IL-1β and IL-6 were measured (E). *P<0.05, **P<0.01, ***P<0.001 vs. vehicle (0.05% CMC).</p

Effects of LFE or FSB on rosiglitazone- and pioglitazone-induced adipocyte differentiation.

<p>3T3-L1 cells were treated with rosiglitazone (50 μM) or pioglitazone (10 μM) in the presence or absence of LFE (10 μg/ml, A-C) or FSB (1 μg/ml, D-F). Six days after the induction of adipocyte differentiation, cells were stained with Oil Red O solution and visualized under an optical microscope (A and D). Absorbance at 490 nm of solutions eluted after Oil Red O staining was used to quantify the extent of adipocyte differentiation (B and E). The mRNA expressions of PPARγ target genes were determined by qPCR (C and F). Experiments were repeated three times in triplicate, and results are presented as means ± SDs. #P<0.05 vs. control; *P<0.05, **P<0.01, ***P<0.001 vs. rosiglitazone or pioglitazone alone.</p

Effects of LFE on hepatic steatosis in KKAy mice.

<p>After 8 weeks of LFE administration, plasma levels of ALT and AST, and TG were determined using commercial kits (A). Liver tissues were frozen and tissue sections were stained with H&E or Oil Red O, and examined under an optical microscope (B). Hepatic TG contents were measured using commercial kit (C). Plasma levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) were measured using ELISA kits (D). Hepatic mRNA levels of IL-1β and IL-6 were measured (E). *P<0.05, **P<0.01, ***P<0.001 vs. vehicle (0.05% CMC).</p