Anti-inflammatory activity of polysaccharides from Phellinus linteus by regulating the NF-κB translocation in LPS-stimulated RAW264.7 macrophages.

Inflammatory response remains one of the most common and serious complications of disease. In order to profound understanding relationship between Phellinus linteus polysaccharides (TCM) and inflammation, inflammatory cell model was constructed by LPS acting RAW264.7 cell line. The results showed that TCM could decrease the pro-inflammatory cytokines (TNF-α, IL-1ß, IL-2, IL-6 and IL-12) contents and the mRNA expression levels and increase the anti-inflammatory cytokines (IL-4 and IL-10) contents and the mRNA expression levels. Additionally, the levels of NF-κB translocation was significantly decreased, which associated with the IκBα phosphorylation level decreased and the AMPKα phosphorylation level increased. These results indicated that TCM could reduce the inflammatory responses in the LPS induced inflammatory cell model might be related to inhibit NF-κB translocation and regulate the balance of anti-inflammatory and pro-inflammatory factors.

Nuciferine Prevents Hepatic Steatosis by Regulating Lipid Metabolismin Diabetic Rat Model.

OBJECTIVE: This study investigatesthe nuciferine capacity to regulate the liver's lipid metabolism regarding steatosis and injury in STZ-induced diabetic rats. MATERIALS AND METHODS: The rats were randomly divided into groups control, diabetic and nuciferine 200 mg/kg/ day treatment. After 4 days of STZ injection, the nuciferine group was treated and administered via oral gavages for 4 weeks. At the end of experiment, blood, liver, myocardial and muscular samples were collected. RESULTS: Nuciferine-treated significantly increased the body weight from 339.4g to 367.8g, but significantly decreased the food and water intake compared with diabetic rats. Also, the nuciferine-treated rats had significantly decreased TC, TG, and FFAs in the liver compared with the diabetic group, especially the serum markers of blood glucose. These were associated with the gene expression related to lipogenesis which was significantly down-regulated; the gene expression involved in lipolysis and fatty acid ß-oxidation was significantly up-regulated. Discussion and. CONCLUSION: The data provide evidence that nuciferine supplementation could protect the liver by regulating lipid metabolism gene expression resulting in decreasing the steatosis and injury in diabetic rat. Thus, nuciferine could be developed as a diabetic adjuvant food additive in future.

Curcumin supplementation regulates lipid metabolism in broiler chickens.

The purpose of this study was to investigate whether dietary curcumin affects lipid metabolism in the liver of broiler chickens. Four treatment groups were formed from 1200 1-day-old broiler chickens, including a base diet (control, supplemented with 0 mg/kg curcumin), 500 mg/kg, 1,000 mg/kg, and 2,000 mg/kg dietary curcumin, for 49 d. At the end of experiment, each group of 50 chickens were sampled and analyzed. Compared with the control group, the results have showed that body weight, average daily weight gain, absolute and relative liver weight significantly decreased in the 1,000 and 2,000 mg/kg curcumin groups (P < 0.05). The absolute and relative abdominal fat weight were significantly decreased in the 2,000 mg/kg curcumin group (P < 0.05). The concentrations of plasma low-density lipoprotein cholesterol (P < 0.05) and plasma and hepatic triglyceride concentrations (P < 0.01) were markedly decreased in the 2,000 mg/kg curcumin group. The hepatic nonesterified fatty acid concentration (P < 0.05) and the hepatic glycogen (P < 0.05) and liver hepatic lipase activities (P < 0.01) were significantly increased in the 1,000 and 2,000 mg/kg curcumin groups. The plasma-free triiodothyronine and thyroxine concentrations were significantly increased in the 2,000 mg/kg curcumin group (P < 0.05). The gene expression levels of fatty acid synthase (FAS) and sterol regulatory element binding protein-1c (SREBP-1c) were significantly decreased in all curcumin groups (P < 0.05), but the gene expression levels of acetyl CoA carboxylase (ACC) and ATP-citrate lyase (ACLY) were significantly decreased only in the 2,000 mg/kg curcumin group (P < 0.05). The expression levels of peroxisome proliferators-activated receptor α (PPARα) and carnitine palmitoyl transferase-I (CPT-I) were significantly increased in the 1,000 and 2,000 mg/kg curcumin groups (P < 0.05). These results indicated that curcumin plays an important role in reduction abdominal fat deposition by decreasing the hepatic and plasma lipid profile and affecting the expression levels of genes related to lipogenesis and lipolysis including ACC, FAS, SREBP-1c, ACLY, PPARα, and CPT-I.

Curcumin alleviates liver oxidative stress in type 1 diabetic rats.

The aim of the present study was to determine the effects of curcumin on antioxidants using a rat model of type 1 diabetes. Seven­week­old male Sprague­Dawley rats were injected with Streptozotocin (STZ) intraperitoneally to induce this model, and then treated with 1.0% curcumin (weight ratio) mixed in their diet for 21 days. The present study included three groups: Control group (NC), diabetic rat model group (DC) and a curcumin treated group (Diab­Cur). The results demonstrated that curcumin treatment markedly decreased the blood glucose levels, plasma malondialdehyde concentration and plasma activity of glutathione peroxidase (GSH­Px) and catalase (CAT); however, it increased the plasma superoxide dismutase (SOD) and insulin levels. Curcumin treatment increased the expression of the CAT, GSH­Px, HO­1 and norvegicus NAD(P)H quinone dehydrogenase 1, and decreased the SOD1 expression, which, led to a diminished oxidative stress status. In addition, curcumin treatment significantly increased the protein expression of Keap1 in the Diab­Cur group when compared with the DC group, decreased cytosolic concentrations of Nrf2 while increasing nuclear accumulation of Nrf2. The results provide evidence that oxidative stress in the STZ­induced diabetic rat model may be attenuated by curcumin via the activation of the Keap1­Nrf2­ARE signaling pathway, as evidenced by a decrease in the blood glucose concentration and an increase in the transcription of several antioxidant genes.