ABSTRACT
AIM: To observe the change of TNF-? mRNA in hypertrophic cardiac myocytes induced by pressure overload in rats and the effect of captopril. METHODS: Serum and heart were collected 42 days after the cardiac hypertrophy model made by pressure overload by abdomen aorta-constriction (AC). Hypertrophic parameter and the concentration of TNF-? in serum and left ventricle were determined by ELISA. TNF-? mRNA in cardiac myocytes was determined by in situ hybridization and analyze by ELIA image analysis system. The orientation of (TNF-?) mRNA in cardiac myocytes was also observed. RESULTS: Left ventricle hypertrophy was observed 42 days after operation. TNF-? mRNA in AC group elevated 98% compared to sham-operated group and descended 64.14% by captopril ((P
ABSTRACT
The inhibitory effect of the crude phycoerythrin(PE) on the frequency of PCE micronucleus induced by CP and its antitumor effect on mice bearing S 180 sarcoma were studied. The result showed that the PE could decrease significantly the frequency of PCE micronucleus with a fair dose-effect relationship, and showed obvious antitumor effect on S 180 bearing mice with an inhibitory rate 44%.
ABSTRACT
AIM: To identify the down-regulated genes in adult rat cardiac fibroblasts (CF) stimulated with angiotensin Ⅱ (AngⅡ). METHODS: Suppression subtractive hybridization (SSH) was performed between the CF stimulated by AngⅡ (driver) and unstimulated CF (tester) to generate subtractive cDNA library. The library was screened with dot blots hybridization to further verify the differentially expressed cDNA clones. Partial positive clones were sequenced and BLAST analyzed. RESULTS: Seventeen down-regulated genes related to intracellular signal transduction, transcriptional repression, deposition of fibrous matrix and cellular cytoskeletal rearrangement, and 4 new expression sequence tags (EST) were acquired. CONCLUSION: SSH is a powerful technique with high sensitivity for the detection and clone of down-regulated genes expressed in CF induced by AngⅡ, which is helpful to clarify the mechanism of cardiac remodeling.