To isolate the specific genes in protoscoleses (PSC) of Echinococcus granulosus under oxidative stresses from the SSH library constructed in the previous study, the gene expression in PSC under oxidative stresses was studied by using real-time PCR. The previously amplified library was sequenced and analyzed in GenBank with Blast research. Sequence analysis indicated that all clones in the SSH library contained the coding sequences, of which some clones showed homology in the GenBank and others were unknown. Differential expression of 4 genes randomly selected and the TPx gene in this library were studied with real-time PCR. It was demonstrated that the gene expression of S88 and H32-1 in oxidative tissues was 2.0 and 2.3 times higher than the un-oxidative stresses respectively. The TPx gene was up-regulated when PSC was induced with H_2H_2 of more than 0.8 mmol/L. These results implies that the up-regulated expression of the above-mentioned genes may be related with the related functions of anti-oxidative process in PSC and they may be used as the candidate genes for the study of anti-oxidation of E.granulosus.

ObjectiveTo explore how hyperthyroidism induces ventricular remodeling via activating β-catenin/FoxO1 in rat cardiomyocytes. MethodsHyperthyroidism-induced ventricular remodeling rat models were established by intraperitoneal injection of levothyroxine （T4） at 0.1 mg/kg for 30 days. β-catenin inhibitor MSAB （14 mg/kg） was administrated for 30 days. We used western blot to detect the expression of myocardial hypertrophy marker ANP， β-catenin and FoxO1； immunofluorescence to examine the expression and intracellular distribution of β-catenin and FoxO1. Hyperthyroidism-induced cardiomyocyte hypertrophy rat models were established by treatment of triiodothyronine （T3） into cultured primary neonatal rat cardiomyocytes for 24 hours. β-catenin siRNA （30 nmol/L） was used to down-regulate β-catenin expression in cardiomyocytes. Western blot and immunofluorescence were used to analyze the effects of β-catenin inhibition on the hyperthyroidism-induced cardiomyocyte hypertrophy. ResultsFollowing Wnt/β-catenin activation， β-catenin was found increased nuclear expression， to bind to the nuclear transcriptional factors and regulate the gene expression. β-catenin nuclear expression was significantly increased in the hyperthyroidism-induced ventricular remodeling rats， but no change was found in the expression of typical transcriptional factor TCF7l2. Our results revealed that inhibiting β-catenin by MSAB attenuated the hyperthyroidism-induced rat ventricular remodeling. Further analysis indicated that β-catenin/FoxO1 expression was significantly increased in hyperthyroidism-induced myocardial hypertrophy which could be attenuated by suppressing β-catenin/FoxO1 in cardiomyocytes. Conclusionsβ-catenin/FoxO1 is activated in hyperthyroidism-induced myocardial hypertrophy and β-catenin/FoxO1 inhibition attenuates hyperthyroidism-induced cardiomyocyte hypertrophy.