Our aim was to investigate whether hot water extract (CLW) of Curcuma longa L. could prevent non-alcoholic fatty liver disease (NAFLD). HepG2 cells were treated with free fatty acid (FFA) mixture (oleic acid: palmitic acid, 2:1) for 24 h to stimulate in vitro fatty liver. In addition, C57BL/6 mice were fed 60 kcal% high-fat (HF) diet for eight weeks to induce fatty liver in vivo. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) productions were increased by FFA and HF-diet, but supplementation with CLW significantly decreased these levels. CLW treatment ameliorated antioxidant activities that were suppressed by exposure to the FFA and HF-diet. Cluster of differentiation 36 (CD36) and fatty acid transport proteins (FATP2 and FATP5) were increased in HF-diet groups, while CLW suppressed their expression levels. Moreover, sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-coenzyme A carboxylase (ACC), and fatty acid synthase (FAS) expression levels were down-regulated in the CLW groups compared to HF-diet groups. On the other hand, 5′ adenosine monophosphate-activated protein kinase (AMPK), Peroxisome proliferator-activated receptor alpha (PPAR-α), and carnitine palmitoyltransferase 1 (CPT-1) expressions were up-regulated in the CLW groups. HF-diet fed mice showed high hepatic triglycerides (TG) content compared to the normal diet mice. However, the administration of CLW restored the hepatic TG level, indicating an inhibitory effect against lipid accumulation by CLW. These results suggest that CLW could be a potentially useful agent for the prevention of NAFLD through modulating fatty acid uptake.

Dexamethasone (DEX) promotes proteolysis, which causes muscle atrophy. Muscle atrophy is connected to sarcopenia. We evaluated the effect of Curcuma longa L. water extract (CLW) on DEX-induced muscle atrophy. ICR mice were divided into three groups (eight mice per group) to investigate the capability of CLW in inhibiting muscle atrophy. The control group (Ex-CON) was administered distilled water (DW) by gavage and subjected to exercise; the muscle atrophy group (Ex-DEX) was administered DW by gavage, an injection of DEX (1 mg/kg body weight/day) intraperitoneally (IP), and subjected to exercise; and the treatment group (Ex-CLW) was administered CLW (1 g/kg body weight/day) by gavage, DEX IP injection, and subjected to exercise. Following the injection of DEX, the expression levels of myostatin, MuRF-1, and Atrogin-1 were increased. However, these expression levels were decreased in the Ex-CLW group, thereby leading to the conclusion that CLW inhibits muscle atrophy. ROS (that was overproduced by DEX) decreased antioxidant enzyme activity and increased malondialdehyde (MDA) levels, which led to muscle atrophy. When CLW was ingested, the antioxidant enzyme activities increased while the MDA levels decreased. These findings suggest that CLW could serve as a natural product for the prevention of muscle atrophy by modulating muscle atrophy-related genes and increasing antioxidant potential.

Gallic acid glycoside was enzymatically synthesized by using dextransucrase and sucrose from gallic acid. After purification by butanol partitioning and preparative HPLC, gallic acid glucoside was detected at m/z 355 (C13, H16, O10, Na)+ by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. The yield of gallic acid glucoside was found to be 35.7% (114 mM) by response surface methodology using a reaction mixture of 319 mM gallic acid, 355 mM sucrose, and 930 mU/mL dextransucrase. The gallic acid glucoside obtained showed 31% higher anti-lipid peroxidation and stronger inhibition (Ki = 1.23 mM) against tyrosinase than that shown by gallic acid (Ki = 1.98 mM). In UVB-irradiated human fibroblast cells, gallic acid glucoside lowered matrix metalloproteinase-1 levels and increased the collagen content, which was indicative of a stronger anti-aging effect than that of gallic acid or arbutin. These results indicated that gallic acid glucoside is likely a superior cosmetic ingredient with skin-whitening and anti-aging functions.

We examined the efficacy of fermented Curcuma longa L. (FT) on the development of alcoholic fatty liver in mice and investigated the underlying mechanism. The protective potential of FT against ethanol-induced fatty liver was determined using C57BL/6 male mice allocated into four groups (8 mice/group). Control groups received either distilled water or 5 g/kg body weight (b.w.) per day ethanol for 8 days. Treatment groups were administered either 300 mg/kg b.w. per day of milk thistle or FT before receiving ethanol. FT contained a higher amount of caffeic acid and tetrahydrocurcumin than C. longa . FT pretreatment significantly suppressed the elevated hepatic lipid droplets associated with ethanol ingestion. In comparison with ethanol-treated control, FT pretreated mice showed inhibited cytochrome P4502E1 (CYP2E1), sterol regulatory element-binding protein-1 (SREBP-1c), and acetyl-CoA carboxylase production but elevated AMP-activated protein kinase, peroxisome proliferator-activated receptor-alpha (PPAR- α ), and carnitine palmitoyltransferase 1 (CPT-1) levels. Taken together, FT is a promising hepatoprotectant for preventing of alcoholic fatty liver through modulating fatty acid synthesis and oxidation.

For this research article, we investigated the protective effects of enzyme-treated caviar powder extract (CV) in ultraviolet B (UVB)-irradiated hairless mice and keratinocytes by confirming moisturizing-related factors and elasticity-related factors. UVB irradiation induced wrinkle formation, dehydration, oxidative stress, and inflammation in the dorsal skin of mice; however, these were suppressed in the CV-supplemented groups in UVB-irradiated hairless mice. Furthermore, in UVB-irradiated keratinocytes, CV treatment increased the antioxidant enzyme activities and the levels of sphingomyelin and hyaluronic acid and decreased the production of pro-inflammatory cytokines and the expression of IkB-α and p65 phosphorylation. These findings indicate that CV can directly protect keratinocytes against UVB irradiation-induced oxidative stress and inflammation. Therefore, we suggest that CV can protect against UVB-induced skin photoaging. Therefore, we suggest that caviar is effective for skin health by preventing UVB-induced skin photoaging.

The objective of this study was to investigate the effect of low-molecular-weight fish collagen (valine-glycine-proline-hydroxyproline-glycine-proline-alanine-glycine; LMWCP) on H₂O₂- or LPS-treated primary chondrocytes and monoiodoacetate (MIA)-induced osteoarthritis rat models. Our findings indicated that LMWCP treatment exhibited protective effects by preventing chondrocyte death and reducing matrix degradation in both H₂O₂-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. This was achieved by increasing the levels of aggrecan, collagen type I, collagen type II, TIMP-1, and TIMP-3, while simultaneously decreasing catabolic factors such as phosphorylation of Smad, MMP-3, and MMP-13. Additionally, LMWCP treatment effectively suppressed the activation of inflammation and apoptosis pathways in both LPS-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. These results suggest that LMWCP supplementation ameliorates the progression of osteoarthritis through its direct impact on inflammation and apoptosis in chondrocytes.