• anti‐obesity assays
• de novo methods
• enzymatic hydrolysis
• obesity
• peptides

• Peptides/chemistry
• Peptides/pharmacology
• Peptides/chemical synthesis
• Anti-Obesity Agents/chemistry
• Anti-Obesity Agents/economics
• Anti-Obesity Agents/pharmacology
• Humans
• Obesity/drug therapy
• Animals

• antibiotics
• fat index
• high-fat diet
• lipid metabolism
• obesity
• oxidative damage

Drug repurposing is a simple concept with a long history, and is a paradigm shift that can significantly reduce the costs and accelerate the process of bringing a new small-molecule drug into clinical practice. We attempted to uncover a new application of spiramycin, an old medication that was classically prescribed for toxoplasmosis and various other soft-tissue infections; specifically, we initiated a study on the anti-inflammatory capacity of spiramycin. For this purpose, we used murine macrophage RAW 264.7 as a model for this experiment and investigated the anti-inflammatory effects of spiramycin by inhibiting the production of pro-inflammatory mediators and cytokines. In the present study, we demonstrated that spiramycin significantly decreased nitric oxide (NO), interleukin (IL)-1β, and IL-6 levels in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Spiramycin also inhibited the expression of NO synthase (iNOS), potentially explaining the spiramycin-induced decrease in NO production. In addition, spiramycin inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs); extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase (JNK) as well as the inactivation and subsequent nuclear translocation of nuclear factor κB (NF-κB). This indicated that spiramycin attenuates macrophages’ secretion of IL-6, IL-1β, and NO, inducing iNOS expression via the inhibition of the NF-κB and MAPK signaling pathways. Finally, we tested the potential application of spiramycin as a topical material by human skin primary irritation tests. It was performed on the normal skin (upper back) of 31 volunteers to determine whether 100 μM and μM of spiramycin had irritation or sensitization potential. In these assays, spiramycin did not induce any adverse reactions. In conclusion, our results demonstrate that spiramycin can effectively attenuate the activation of macrophages, suggesting that spiramycin could be a potential candidate for drug repositioning as a topical anti-inflammatory agent.

• drug repurposing
• inflammation
• macrophages
• mitogen-activated protein kinase (MAPK)
• nuclear factor κB (NF-κB)
• spiramycin

The global obesity epidemic has nearly doubled since 1980, and this increasing prevalence is threatening public health. It has been reported that natural products could contain potential functional ingredients that may assist in preventing obesity. Bojungchiseub-tang (BJT), mentioned in the Donguibogam as an herbal medication for the treatment of edema, a symptom of obesity, consists of eleven medicinal herbs. However, the pharmacological activity of BJT has not been investigated. The present study was designed to investigate the putative effect of BJT on the adipogenesis of 3T3-L1 cells and the weight gain of high-fat diet (HFD-) fed C57BL/6 mice. Oil Red O staining was conducted to examine the amount of lipids in 3T3-L1 adipocytes. Male C57BL/6 mice were divided into three groups: standard diet group (control, CON), 45% HFD group (HFD), and HFD supplemented with 10% of BJT (BJT). The expression levels of genes and proteins related to adipogenesis in cells, WAT, and liver were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot, respectively. We found that BJT treatment significantly decreased the protein and mRNA levels of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), and sterol regulatory element-binding protein 1 (SREBP1) in a dose-dependent manner in differentiated 3T3-L1 cells. Similar to the results of the in vitro experiment, BJT suppressed HFD-induced weight gain in an obese mouse model. In addition, BJT effectively reduced the HFD-induced epididymal adipose tissue weight/body weight index. BJT also downregulated the mRNA levels of PPARγ, C/EBPα, and SREBP1 in the epididymal adipose and liver tissue of HFD-fed obese mice. These findings suggest that BJT induces weight loss by affecting adipogenic transcription factors.

• derivatives
• tachyzoite
• usnic acid

• Animals
• Antiprotozoal Agents/administration & dosage
• Antiprotozoal Agents/chemical synthesis
• Antiprotozoal Agents/chemistry
• Benzofurans/administration & dosage
• Benzofurans/chemical synthesis
• Benzofurans/chemistry
• Drug Evaluation, Preclinical
• Female
• HeLa Cells
• Humans
• Mice
• Molecular Structure
• Toxoplasma/drug effects
• Toxoplasma/growth & development
• Toxoplasmosis/drug therapy
• Toxoplasmosis/parasitology

• Adipogenesis
• Antimicrobial agents
• Bone marrow mesenchymal stem cells
• Chondrogenesis
• Osteogenesis

• Adenovirus
• Adiposity
• Animal
• Human
• Infectobesity
• Pawnobe
• Transmissible Spongiform Encephalopathy

• Adenoviridae Infections/complications
• Animals
• Bacteriophages/pathogenicity
• Disease Models, Animal
• Forecasting
• Herpesviridae Infections/complications
• Humans
• Obesity/therapy
• Obesity/virology
• Prion Diseases/complications
• Virus Diseases/complications