To establish mouse endometrial injury model by curettage or coagulation.Female ICR mice were randomly allocated into 2 groups: in curettage group, a blunt 20G needle was inserted in one uterine horn with 0.05 megapascals negative pressure; in coagulation group, one uterine horn was coagulated using a monopolar electric needle with 0.5 watts power. In both groups the contra-lateral uterine horn was used as control. The morphological changes and thickness of endometrium were evaluated 1 week after operation. The endometrial samples were taken on d4 of pregnancy, and the expressions of endometrial receptivity-related cytokines were examined. The number of implanted embryos on each side of uterus was calculated on d10 of pregnancy.There was no difference in operation time between 2 groups. In both groups, the endometrial glands and stroma were significantly reduced, and the endometrial thickness was also significantly decreased on injury side compared to contra-lateral horn. However, local injury was more severe in coagulation group, uterine obliteration and hydrops were developed in 2 mice of coagulation group, and none in curettage group. The expressions of leukemia inhibitory factor (LIF) and oncostatin M (OSM) were significantly reduced on injured side in both groups compared to opposite side; however, the expression of LIF and OSM in curettage group was higher than that in coagulation group. The numbers of implanted embryos were decreased in both groups on injured side compared to opposite side, and fetal death was only observed in coagulation group.Both curettage and coagulation can make injury on mouse endometrium, impair endometrial receptivity and reduce fertility. Curettage can cause moderate injury, and coagulation may lead to more severe injury.

The aim of this paper was to investigate the mechanism of the active peptide DP17 of Eupolyphaga steleophaga in the treatment of hyperlipidemia rats. HPLC and MADIL-TOF/TOF-MS were used for the amino acid sequence analysis and solid-phase synthesis on the active peptide of E. steleophaga which were obtained by biomimetic enzymatic hydrolysis, separation and purification. The hyperlipidemia model was established by feeding with high-fat diet.Twenty days later, the rats in the blank group and the model group were given the saline and the rats in remaining groups were given the corresponding drugs by oral administration. After administration for 4 weeks, the levels of triglyceride(TG), total cholesterol(TC) and low density lipoprotein(LDL) in serum, the levels of TG, TC, adenosine monophosphate(AMP), adenosine triphosphate(ATP) in liver tissues and TG in feces were detected, respectively. Hematoxylin-eosin(HE) staining was used to observe the pathological changes of liver tissues. The Real-time fluorescence quantitative PCR method was used to detect the expression of acetyl coa carboxylase(ACC) and hydroxymethylglutaryl-coa reductase(HMGCR) mRNA in liver tissues. The expression of mammalian target of rapamycin(mTORC1) protein and adenosine 5'-monophosphate-activated protein kinase(AMPK) in liver tissues were detected by Western blot. The analysis showed that the amino acid sequence of active peptide from E. steleophaga was DAVPGAGPAGCHPGAGP(DP17). The results of pharmacological experiments showed that after oral administration of DP17 in rats, the levels of TG, TC and LDL in serum as well as TG and TC levels in liver tissues were significantly decreased(P<0.05), while the levels of AMP, ATP in liver tissues and TG content in feces were significantly increased(P<0.05); the liver steatosis of rats was significantly relieved; the expression of ACC, HMGCR mRNA and mTORC1 protein in liver tissues were significantly reduced, while the expression of AMPK phosphorylated protein was significantly increased(P<0.05). DP17, the active peptide of E. steleophag can significantly reduce lipid accumulation in liver tissues, and it may play a role in reducing blood lipids by regulating the energy metabolism balance in the body and activating AMPK/mTOR signaling pathway.
Animals ; Diet, High-Fat/adverse effects* ; Hyperlipidemias/genetics* ; Lipids ; Liver ; Peptides ; Rats ; Triglycerides