Recent findings on the association of gut microbiota with various diseases, including obesity, prompted us to investigate the possibility of using a certain type of gut bacteria as a safe therapeutic for obesity. Lactobacillus mutants with enhanced capacity in absorption of free fatty acids ( FFA s) were isolated to show reduced absorption of FFA s by the administered host, attributing to inhibition of body weight gain and body fat accumulation as well as amelioration of blood profiles. Consequently, high throughput screening of natural FFA s‐absorbing intestinal microbes led to the isolation of Lactobacillus reuteri JBD 30 l. The administration of Lactobacillus JBD 30l lowered the concentration of FFA s in the gut fluid content of small intestine, thus reducing intestinal absorption of FFA s whereas promoting fecal excretion of FFA s. Animal data also confirmed that the efficacy of Lactobacillus JBD 30l on body weight similar to that of orlistat, an FDA ‐approved pharmaceutical for long‐term use to treat obesity. In a subsequent random, double‐blind, placebo‐controlled clinical trial ( KCT 0000452 at Clinical Research Information Service of Korea), there was a statistically significant difference in the percentage change in body weight between the Lactobacillus JBD 301 and the placebo group ( P = 0.026) as well as in the BMI ( P = 0.036) from the 0‐week assessment to the 12‐week assessment. Our results show that FFA ‐absorbing Lactobacillus JBD 301 effectively reduces dietary fat absorption, providing an ideal treatment for obesity with inherent safety.

Apigenin, a flavonoid abundant in various vegetables and fruits, including parsley and onions, has been reported to possess anticarcinogenic effects. However, the direct molecular target of apigenin and its chemopreventive effect on ultraviolet (UV)-induced skin inflammation are not understood fully. Herein, we examined the anti-inflammatory effect of apigenin and its associated mechanisms in JB6 P+ cell line and SKH-1 hairless mouse model. Apigenin inhibited UVB-induced cyclooxygenase-2 (COX-2) expression, which is a well-known key mediator of inflammation and cancer, and restored the upstream stimulatory factor level in JB6 P+ cells. Immunoblot and kinase assay data demonstrate that Src activity was attenuated by apigenin, and this led to subsequent inhibition of UVB-induced phosphorylation of epidermal growth factor receptor, mitogen-activated protein kinases and Akt signaling. Inhibitory effects of apigenin on UVB-induced signaling were also confirmed in HaCaT human keratinocytes. In addition, in vitro pull-down assays revealed that apigenin binds Src in an adenosine triphosphate-competitive manner. Results using in vivo skin model indicate apigenin significantly inhibits UVB-induced ear edema development, COX-2 expression and Src kinase activity in SKH-1 hairless mice. Collectively, these findings suggest that apigenin exerts potent chemopreventive activity against UVB-induced skin inflammation primarily by targeting Src.

Multiple lines of evidence suggest that natural compounds can prevent skin ageing induced by ultraviolet light. Luteolin, a bioactive compound found in chilli, onion, broccoli, celery and carrot, has been reported to exhibit anti-photoageing effects in vitro. However, the molecular targets and mechanisms of luteolin are still poorly understood. In this study, we sought to investigate the effects of luteolin on UVB-induced photoageing and the molecular mechanisms involved, using HaCaT human keratinocytes and SKH-1 hairless mice. Luteolin was found to inhibit UVB-induced MMP-1 expression in HaCaT cells, as well as UVB-induced activation of AP-1, a well-known transcription factor targeting the MMP-1 promoter region, as well as c-Fos and c-Jun, which comprise the AP-1 complex. In contrast, Western blot data showed that UVB-induced phosphorylation of JNK, ERK and p90RSK was not inhibited by luteolin. In vitro kinase assay data revealed that luteolin significantly suppressed JNK1 and p90RSK activity, but not that of JNK2 and ERK2. Pull-down assays showed that luteolin binds JNK1 in an ATP-competitive manner and p90RSK2 in an ATP-independent manner. Luteolin also inhibited UVB-induced wrinkle formation and MMP-13 expression, a rodent interstitial collagenase in mouse skin, in vivo. Taken together, our observations suggest that luteolin exhibits anti-photoageing effects in vitro and in vivo and may have potential as a treatment for the prevention of skin ageing.

Zingiber officinale Roscoe, one of the most widely used spices, has been reported to have anti‐obesity and anti‐diabetes effects. In the present study, we investigated the effects of 6‐shogaol, a bioactive compound present in ginger, on the adipogenic process in 3T3‐L1 preadipocytes. The anti‐adipogenic effects of 6‐shogaol was significantly higher than the more widely investigated 6‐gingerol, another major ginger constituent. We observed that 6‐shogaol inhibited the expression of two master regulators of adipogenesis, PPARγ and C/EBPα, and also stimulated lipolysis in mature 3T3‐L1 adipocytes. Collectively, these results suggest that 6‐shogaol, not 6‐gingerol, is the major compound present in ginger responsible for its reported anti‐adipogenic properties. Practical Applications Ginger is widely consumed all over the world, and has been associated with various health benefits. At least some of these benefits have been previously attributed to 6‐gingerol. In the present study, we observed that 6‐shogaol has more potent anti‐adipogenic effects than 6‐gingerol in 3T3‐L1 cells. This is the first study to investigate the anti‐obesity effect of 6‐shogaol in vitro, and provides a new perspective on future development of ginger‐based anti‐obesity strategies.

Our results suggest that 6,7,4'-THIF suppresses adipogenesis in 3T3-L1 preadipocytes by directly targeting PI3K. Soy isoflavones like 6,7,4'-THIF may have potential for development into novel treatment strategies for chronic obesity.