Effect of lead acetate on the apoptosis and the expression of bcl-2 and bax genes in rat brain cells / 中华预防医学杂志

<p><b>OBJECTIVES</b>To explore the effect of lead acetate on the apoptosis of rat brain neural cells and the relationship between the apoptosis and the bcl-2 as well as bax gene expression.</p><p><b>METHODS</b>Lead acetate was given to SD rats by intraperitoneal injection for 5 days at the dosage of 25, 50 and l00 mg/kg body weight respectively. The rates of apoptosis and the expression of bcl-2 (Bcl-2) and bax (Bax) in neural cells from cerebral cortex, hippocampus and carebellum were measured respectively by flow cytometry (FCM).</p><p><b>RESULTS</b>The rates of apoptosis in neural cells from cerebral cortex, hippocampus and cerebellum in every treatment group were significantly higher than that of control (P < 0.01), and there was a significant dose-response relationship (r = 0.998, 0.989 and 0.997 respectively). The expression of bcl-2 was significantly decreased, whereas bax was significantly increased, in neural cells from cerebral cortex, hippocampus and cerebellum in every lead acetate treatment group (FI) compared with the control group, and there was a significant dose-response relationship (r = -0.886, -0.787 and -0.832 respectively for bcl-2, r = 0.971, 0.988 and 0.991 respectively for bax). The value of Bcl-2/Bax in every treatment group decreased significantly compared with control, and there was a nice dose-response relationship (r = -0.863, -0.829 and -0.999, respectively). Correlation analysis showed that rates of apoptosis were inversely correlated with the expression of bcl-2 (r = -0.750, -0.509, and -0.667, respectively), whereas positively correlated with the expression of bax (r = 0.748, 0.56l, and 0.668, respectively). And there were inverse correlations between the rates of apoptosis and Bcl-2/Bax expression.</p><p><b>CONCLUSION</b>Lead may induce apoptosis in rat brain neural cells through the down regulation of bcl-2 and the up regulation of bax gene expression.</p>

Integrin ?_3-FAK pathway is involved in neointima formation / 中国病理生理杂志

AIM: To investigate whether the expression of integrin ?_3 and the activation of focal adhesion kinase(FAK) are involved in neointima formation after de-endothelium.METHODS: The model of intima hyperplasia was prepared by balloon injury.The levels of osteopontin(OPN),integrin ?_3 and FAK in vascular tissue were detected by Western blotting and immunohistochemistry.RESULTS: There were similar expression patterns in OPN,integrin ?_3 and FAK following balloon injury.The levels of three proteins were markedly increased 3 days after operation and reached the peak at 7th day.The increased FAK was mainly the phosphorylated form.The migration and proliferation of vascular smooth muscle cells was associated with the increase in the expression of integrin ?_3 and FAK,and was parallel with rapid turnover of extracellular matrix(ECM).CONCLUSION: The interaction of cells with ECM mediated by OPN and integrin ?_3 is essential for migration.The integrin ?_3-FAK pathway is involved in neointima formation.

Changes of contractile protein expression and its effect on vessel contraction during neointimal formation / 中国病理生理杂志

AIM: To determine the relationship between the changes of SM ?-actin and SM22? expression and vascular tone. METHODS: The expression of SM ?-actin and SM22? during restenosis after de-endothelialization were detected by Western blotting and immunohistochemistry. The structure of myofilaments was observed by transmission electron microscopy. The vascular contraction induced by phenylephrine was measured by a force transducer. RESULTS: The levels of SM ?-actin and SM22? expression in vascualar wall declined after de-endothelialization. The myofilaments in VSMC were modulated from well arranged and dense bundles to discrete network. However, the vascular tone and reactivity to agonist were much higher than that in control (P