To investigate the functional effects of probiotic treatment on the gut microbiota, as well as liver and adipose gene expression in diet-induced obese mice. Male C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce obesity, and then randomized to receive HFD+probiotic (Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, n = 9) or HFD+placebo (n = 9) for another 10 weeks. Normal diet (ND) fed mice (n = 9) served as non-obese controls. Diet-induced obese mice treated with probiotics showed reduced body weight gain and fat accumulation as well as lowered plasma insulin, leptin, total-cholesterol and liver toxicity biomarkers. A total of 151,061 pyrosequencing reads for fecal microbiota were analyzed with a mean of 6,564, 5,274 and 4,464 reads for the ND, HFD+placebo and HFD+probiotic groups, respectively. Gut microbiota species were shared among the experimental groups despite the different diets and treatments. The diversity of the gut microbiota and its composition were significantly altered in the diet-induced obese mice and after probiotic treatment. We observed concurrent transcriptional changes in adipose tissue and the liver. In adipose tissue, pro-inflammatory genes (TNFα, IL6, IL1β and MCP1) were down-regulated in mice receiving probiotic treatment. In the liver, fatty acid oxidation-related genes (PGC1α, CPT1, CPT2 and ACOX1) were up-regulated in mice receiving probiotic treatment. The gut microbiota of diet-induced obese mice appears to be modulated in mice receiving probiotic treatment. Probiotic treatment might reduce diet-induced obesity and modulate genes associated with metabolism and inflammation in the liver and adipose tissue.

Objective: To determine the effects of naturally derived probiotic strains individually or combination on a short‐term diet‐induced obesity model.Design and Methods: C57BL/6J mice (n = 50) were randomly divided into five groups, then fed a high‐fat high‐cholesterol diet (HFCD), HFCD and Lactobacillus plantarum KY1032 (PL, 10¹⁰cfu/day), HFCD and Lactobacillus curvatus HY7601 (CU, 10¹⁰cfu/day), HFCD and in combination with PL+CU (10¹⁰cfu/day), or a normal diet (ND) for 9 weeks.Results: PL and CU showed distinct and shared metabolic activity against a panel of 50 carbohydrates. Fat accumulation in adipose tissue and liver was significantly reduced by probiotic strains CU or PL+CU. Probiotic strains CU or PL+CU reduced cholesterol in plasma and liver, while PL+CL had a synergistic effect on hepatic triglycerides. Probiotic strains PL+CU combination was more effective for inhibiting gene expressions of various fatty acid synthesis enzymes in the liver, concomitant with decreases in fatty acid oxidation‐related enzyme activities and their gene expressions.Conclusions: Multi‐strain probiotics may prove more beneficial than single‐strain probiotics to combat fat accumulation and metabolic alterations in diet‐induced obesity.

Gyejibokryeong-hwan (GJBRH; Keishi-bukuryo-gan in Japan and Guizhi Fuling Wan in China) is a traditional herbal formula comprising five medicinal herbs and is used to treat climacteric syndrome. GJBRH has been shown to exhibit biological activity against diabetes, diabetic nephropathy, atherosclerosis, ischemia, and cancer. However, there is no scientific evidence of its activities against skin inflammation, including atopic dermatitis. We used the HaCaT human keratinocyte cell line to investigate the effects of GJBRH on skin inflammation. No significant cytotoxicity was observed in cells treated with GJBRH up to a concentration of 1000 µg/mL. Exposure to the proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) significantly increased HaCaT cell production of the following chemokines: macrophage-derived chemokine (MDC)/CCL22; regulated on activation, normal T-cell expressed and secreted (RANTES)/CCL5; and interleukin-8 (IL-8). In contrast, GJBRH significantly reduced the production of MDC, RANTES, and IL-8 compared with control cells simulated with TNF-α and IFN-γ. Consistently, GJBRH suppressed the mRNA expression of MDC, RANTES, and IL-8 in TNF-α and IFN-γ-treated cells. Treatment with GJBRH markedly inhibited phosphorylation of signal transducer and activator of transcription 1 (STAT1) in HaCaT cells stimulated with TNF-α and IFN-γ. Our findings indicate that GJBRH impairs TNF-α and IFN-γ-mediated inflammatory chemokine production and STAT1 phosphorylation in keratinocytes. We suggest that GJBRH may be a potent therapeutic agent for inflammatory skin disorders.

Dendrobii Herba, a traditional Korean medicine, is used for treating atrophic gastritis, diabetes and cardiovascular diseases. Phytochemical studies of Dendrobium species and their compounds have been conducted. However, the pharmaceutical effects of these compounds have not yet been elucidated. We performed quantitative determination of four phenolic compounds, – (1) 4-hydroxybenzoic acid, (2) vanillic acid (3) syringic acid and (4) ferulic acid – in Dendrobii Herba using high-performance liquid chromatography coupled with a photodiode array detector. In addition, we investigated the effects of compounds in LPS-stimulated RAW 264.7 cells by measuring of inflammatory mediators. Among the four compounds, 1–3 had a significant inhibitory effect on TNF-α production. The levels of IL-6 were significantly reduced by treatment with compounds 13 and 4 compared with LPS treated cell. All compounds significantly reduced LPS-stimulated PGE₂ production. Thus, these four marker compounds from Dendrobii Herba exhibit anti-inflammatory activity by targeting different inflammation-related cytokines.

Galkeun‐tang (GKT; Galgen-tang in Chinese and Kakkon-to in Japanese), a traditional herbal formula, has been used for treatment of the common cold. Here, we report in vitro antioxidant and antiadipogenic effects of GKT. GKT increased the activities of scavenging 2,2′‐azinobis‐(3‐ethylbenzothiazoline‐6‐sulfonic acid) (ABTS) and 2,2‐diphenyl‐1‐picrylhydrazyl (DPPH) radicals. GKT also significantly reduced the malondialdehyde (MDA) generation during low‐density lipoprotein (LDL) oxidation and the electrophoretic mobility of oxidized LDL, indicating inhibitory effects of GKT on Cu²⁺‐mediated oxidation of LDL. Regarding antiadipogenic activity, GKT treatment significantly suppressed lipid accumulation, triglyceride production, and glycerol‐3‐phosphate dehydrogenase (GPDH) activity in differentiated 3T3‐L1 adipocytes. Consistent with this, GKT significantly reduced the secretion of leptin, a major adipokine, in differentiated 3T3‐L1 adipocytes. Overall, our findings suggest that GKT has the potential for antioxidative and antiadipogenic properties.