Hepatic lipid deposition is one of the basic manifestations of obesity, and nowadays pharmacological treatment is the most important tool. Punicalagin(PU), a polyphenol derived from pomegranate peel, is a potential anti-obesity substance. In this study, 60 C57BL/6J mice were randomly divided into a normal group and a model group. After establishing a model of simple obesity with a high-fat diet for 12 weeks, the successfully established rat models of obesity were then regrouped into a model group, an orlistat group, a PU low-dose group, a PU medium-dose group, and a PU high-dose group. The normal group was kept on routine diet and other groups continued to feed the high-fat diet. The body weight and food intake were measured and recorded weekly. After 8 weeks, the levels of the four lipids in the serum of each group of mice were determined by an automatic biochemical instrument. Oral glucose tole-rance and intraperitoneal insulin sensitivity were tested. Hemoxylin-eosin(HE) staining was applied to observe the hepatic and adipose tissues. The mRNA expression levels of peroxisome proliferators-activated receptor γ(PPARγ) and C/EBPα were determined by real-time quantitative polymerase chain reaction(Q-PCR), and the mRNA and protein expression levels of adenosine 5'-monophosphate-activated protein kinase(AMPK), anterior cingulate cortex(ACC), and carnitine palmitoyltransferase 1A(CPT1A) were determined by Western blot. Finally, the body mass, Lee's index, serum total glyceride(TG), serum total cholesterol(TC), and low-density lipoprotein cholesterol(LDL-C) levels were significantly higher and high-density lipoprotein cholesterol(HDL-C) levels were significantly lower in the model group as compared with the normal group. The fat deposition in the liver was significantly increased. The mRNA expression levels of hepatic PPARγ and C/EBPα and the protein expression level of ACC were increased, while the mRNA and protein expression levels of CPT-1α(CPT1A) and AMPK were decreased. After PU treatment, the above indexes of obese mice were reversed. In conclusion, PU can decrease the body weight of obese mice and control their food intake. It also plays a role in the regulation of lipid metabolism and glycometabolism metabolism, which can significantly improve hepatic fat deposition. Mechanistically, PU may regulate liver lipid deposition in obese mice by down-regulating lipid synthesis and up-regulating lipolysis through activation of the AMPK/ACC pathway.
Rats ; Mice ; Animals ; Mice, Obese ; AMP-Activated Protein Kinases/metabolism* ; PPAR gamma/metabolism* ; Mice, Inbred C57BL ; Liver/metabolism* ; Obesity/genetics* ; Body Weight ; Lipid Metabolism ; Diet, High-Fat/adverse effects* ; Lipids ; Cholesterol

Objective To establish a quantitative analysis method for determining 99mTc-HYNIC-PEG4-E[PEG4-c(RGDfK)]2 (99mTc-3PRGD2,a radioactive tumor agent)byγcounter, and to investigate the distribution of 99mTc-3PRGD2 in mice bearing with lung carcinoma xenograft. Methods The mice were divided into 4 normal groups and one blocking peptide group(control group). The 99mTc-3PRGD2(8μg/kg)was injected to mice bearing with lung carcinoma xenograft through the tail intravenous administration. Tissues of the normal mice were taken at 0.5,1,2 and 4 h. The control group were treated by 3PRGD2 and 99mTc-3PRGD2. The control mice were injected with the 3PRGD2 saline solution(2.5 mg/ml,0.2 ml)at 0.5 h earlier before the injection of 99mTc-3PRGD2. The tu?mor and organ tissues of the control mice were taken at 2 h. The radioactivity was detected by Gamma Counter. Results The radioac?tivity of 99mTc-3PRGD2 detected was high in the tumor and very low in brain. In addition,high radioactivity in kidneys and bladder sug?gested that the drug excreted by renal. Conclusion The results proved that the blocking peptide can competitively inhibit the combi?nation of 99mTc-3PRGD2 and integrinαvβ3 receptors.