This study investigated the anti-obesity effects of collagen peptide derived from skate skin on lipid metabolism in high-fat diet (HFD)-fed mice. All C57BL6/J male mice were fed a HFD with 60% kcal fat except for mice in the normal group which were fed a chow diet. The collagen-fed groups received collagen peptide (1050 Da) orally (100, 200, or 300 mg/kg body weight per day) by gavage, whereas the normal and control groups were given water (n = 9 per group). The body weight gain and visceral adipose tissue weight were lower in the collagen-fed groups than in the control group (p < 0.05). Plasma and hepatic lipid levels were significantly reduced by downregulating the hepatic protein expression levels for fatty acid synthesis (sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)) and cholesterol synthesis (SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)) and upregulating those for β-oxidation (peroxisome proliferator-activated receptor alpha (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1)) and synthesis of bile acid (cytochrome P450 family 7 subfamily A member 1 (CYP7A1)) (p < 0.05). In the collagen-fed groups, the hepatic protein expression level of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK) and plasma adiponectin levels were higher, and the leptin level was lower (p < 0.05). Histological analysis revealed that collagen treatment suppressed hepatic lipid accumulation and reduced the lipid droplet size in the adipose tissue. These effects were increased in a dose-dependent manner. The findings indicated that skate collagen peptide has anti-obesity effects through suppression of fat accumulation and regulation of lipid metabolism.

Vegetable-based diets have generally focused on their health benefits including negative associations with the serum cholesterol concentrations. The aim of this study was to investigate whether serum lipid concentrations are influenced by the amount of kimchi intake. For the study, 100 volunteers were assigned to 2 dietary groups, low (15 g/day, n = 50) and high (210 g/day, n = 50) kimchi intake, and were housed together in a dormitory for 7 days. Identical meals except with different amount of kimchi were provided and subjects were instructed to maintain their normal physical activity. Concentrations of fasting blood glucose (FBG), total glucose, total cholesterol and low density lipoprotein (LDL)-C significantly decreased in both groups after 7 days of kimchi intake, but the effects were dose dependent. Lipid lowering effects of kimchi were more profound in the subjects with total cholesterol and LDL-C level over 190 and 130 mg/dL, respectively, in both groups. FBG was significantly decreased in the high kimchi intake as compared to the low intake group (P = .003). In conclusion, greater consumption of kimchi improved FBG and serum total cholesterol in young healthy adults.

This study investigated the abilities of kimchi and its bioactive compounds to ameliorate amyloid beta (Aβ)-induced memory and cognitive impairments. Mice were given a single intracerebroventricular injection of Aβ25-35, followed by a daily oral administration of capsaicin (10 mg·kg-bw–1), 3-(4′-hydroxyl-3′,5′-dimethoxyphenyl)propionic acid (50 mg/kg bw), quercetin (50 mg/kg bw), ascorbic acid (50 mg/kg bw), or kimchi methanol extract (KME; 200 mg/kg bw) for 2 weeks (n = 7 per group). Carboxymethylcellulose was used as a vehicle for the normal and control groups. Behavioral task tests showed that the learning and memory abilities were significantly waned by the injected Aβ25-35, but these cognitive deficits were recovered by the administrated KME and kimchi bioactive compounds (p < 0.05). The reactive oxygen species, peroxynitrite, and thiobarbituric acid reactive substances levels were lower, and the glutathione level was higher, in the KME and bioactive compound groups than in the control group (p < 0.05). In the KME and bioactive compound groups, the protein expression levels of antioxidant enzymes (nuclear factor (erythroid-derived 2)-like 2-regulated superoxide dismutase-1 and glutathione peroxidase) were increased, whereas those of inflammation-related enzymes (nuclear factor-kappaB -regulated inducible nitric oxide synthase and cyclooxygenase-2) were decreased (p < 0.05). Thus, the antioxidative and anti-inflammatory properties of bioactive compounds-rich kimchi might help to attenuate the symptoms of Alzheimer’s disease.

This study investigated the inhibitory effects of kimchi bioactive compounds against endoplasmic reticulum (ER) stress-induced apoptosis in amyloid beta (Aβ)-injected mice. Mice received a single intracerebroventricular injection of Aβ, except for the normal group. Mice were subjected to oral administration of 10 mg of capsaicin, 50 mg of 3-(4'-hydroxyl-3',5'-dimethoxyphenyl)propionic acid (HDMPPA), 50 mg of quercetin, 50 mg of ascorbic acid, or 200 mg of kimchi methanol extract (KME) per kilogram of body weight for 2 weeks ( n = 7 per group). In the in vitro blood-brain barrier (BBB) permeability test, all bioactive compounds penetrated the BBB except ascorbic acid. The protein expression level of APP, BACE, and p-Tau elevated by Aβ injection was decreased by kimchi bioactive compounds ( P < 0.05). Quercetin, HDMPPA, and KME decreased oxidative stress, as indicated by ROS and TBARS levels ( P < 0.05). The protein expression level of ER stress markers GRP78, p-PERK, p-eIF2α, XBP1, and CHOP and the proapoptotic molecules Bax, p-JNK, and cleaved caspases-3 and -9 decreased ( P < 0.05). In contrast, the protein expression level of antiapoptotic molecules Bcl2 and cIAP increased ( P < 0.05). These results were supported by histological analysis.

This study was conducted to compare the protective effects of astaxanthin (ASX) with Corni Fructus (CF) against diabetes-induced pathologies such as oxidative stress-induced inflammation and advanced glycation end product (AGE) formation in the liver of type 1 diabetic rats. ASX (50 mg/kg body weight/day) or CF (200 mg/kg body weight/day) was orally administered every day for 18 days to streptozotocin (STZ)-induced diabetic rats, and their effects were compared with nondiabetic and diabetic control rats. The administration of CF, but not ASX, decreased both the elevated serum and hepatic glucose concentration in diabetic rats. In diabetic rats, increased levels of AGE, reactive oxygen species, and lipid peroxidation were significantly decreased by treatment with both ASX and CF in the liver of diabetic rats. STZ treatment markedly augmented the protein expressions of AGE, and both ASX and CF efficiently attenuated these increases in hepatic protein expressions. In addition, oxidative stress and proinflammatory protein expressions were upregulated in the diabetic rats. On the contrary, these upregulations of protein expressions were decreased by the administration of ASX or CF. These results suggest that the inhibitory effect of ASX on diabetes-induced hepatic dysfunction could be derived from the blocking of AGE formation and further anti-inflammation and that CF exhibited beneficial effects through the attenuation of hyperglycemia, and thus the inhibition of AGE formation and the inflammatory responses. Therefore, ASX as well as CF may help prevent ongoing diabetes-induced hepatic injury.

No abstract

The effects of 3-(4'-hydroxyl-3',5'-dimethoxyphenyl)propionic acid (HDMPPA) originating from Korean cabbage kimchi were investigated, showing an antioxidant effect on the prevention of atherosclerosis in hypercholesterolemic rabbits. Twenty-one 3-month-old rabbits were fed an atherogenic diet containing 0.5% (w/w) cholesterol and 10% (w/w) coconut oil, whereas another two groups were given an atherogenic diet with intravenous injection of either HDMPPA or simvastatin (0.33 mg/kg/day) for 4 weeks. HDMPPA inhibited the oxidative modification of low-density lipoprotein (IC 50 = 1.4 microg/mL) and increased 2,2'-diphenyl-1-picrylhydrazyl radical scavenging activity (IC 50 = 0.78 microg/mL) in a dose-dependent manner. In hypercholesterolemic rabbits, the thickness of intima of aorta of the HDMPPA group was significantly reduced (control versus HDMPPA, 42%; simvastatin, 38%) without a plasma cholesterol-lowering effect. Thiobarbituric acid reactive substance formation in the plasma of the HDMPPA group was significantly decreased compared to that of the control group. Furthermore, the generation of vascular reactive oxygen species in HDMPPA group was suppressed as the cyclooxygenase-2 protein level decreased. These findings suggest that HDMPPA prevents the development of aortic atherosclerosis in high-cholesterol-fed rabbits. The antiatherosclerotic effect of HDMPPA may be due to an antioxidative effect at a low dose without cholesterol-lowering effects.

The protective effects of a chondroitin sulfate-rich extract (CSE) from skate cartilage against lipopolysaccharide (LPS)-induced hepatic damage were investigated, and its mechanism of action was compared with that of chondroitin sulfate (CS) from shark cartilage. ICR mice were orally administrated 200 mg/kg body weight (BW) of CS or 400 mg/kg BW of CSE for 3 consecutive days, followed by a one-time intraperitoneal injection of LPS (20 mg/kg BW). The experimental groups were vehicle treatment without LPS injection (NC group), vehicle treatment with LPS injection (LPS group), CS pretreatment with LPS injection (CS group), and CSE pretreatment with LPS injection (CSE group). Hepatic antioxidant enzyme expression levels in the CS and CSE groups were increased relative to those in the LPS group. In LPS-insulted hepatic tissue, inflammatory factors were augmented relative to those in the NC group, but were significantly suppressed by pretreatment with CS or CSE. Moreover, CS and CSE alleviated the LPS-induced apoptotic factors and mitogen-activated protein kinase (MAPK). In addition, CS and CSE effectively decreased the serum lipid concentrations and downregulated hepatic sterol regulatory element-binding proteins expression. In conclusion, the skate CSE could protect against LPS-induced hepatic dyslipidemia, oxidative stress, inflammation, and apoptosis, probably through the regulation of MAPK signaling.