Using mice infected with coxsackie B-3 virus (CVB3) as a viral myocarditis model, we observed the inhibitory effect of Astragalus membranaceus (AM) on CVB3-RNA replication in myocardial tissue of mice by RNA-RNA in si...Using mice infected with coxsackie B-3 virus (CVB3) as a viral myocarditis model, we observed the inhibitory effect of Astragalus membranaceus (AM) on CVB3-RNA replication in myocardial tissue of mice by RNA-RNA in situ hybridization with negative-strand RNA Probes labelled with ￣(35)S and quantitative imaging analysis of positive signals. The mechanism of its effect on CVB3-RNA replication has been investigated by detection of beta-interferon (β-IFN) as well. Results showed that the copy numbers of CVB3-RNA as well as the histologic scores (necrosis) in myocardial tissues of infected-AM treated mice were significantly lower than those in infected and normal saline treated mice, suggesting that AM could inhibit the replication of CVB3-RVA,but its effect on CVB3-RNA replication had no correlation with induction of β-IFN.展开更多
The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that t...The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<O. 01) by verapamil (1 μmol/L) after infection of heart cells for 48h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (Iμmol/L and 10 nmo/L) at the same time for 48h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<O. 05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e. g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.展开更多
Objective To determine the relationship between remodeling and dysfunct ion of left ventricle (LV) and the expression of the angiotensin AT1 receptor mRNA after myocardial infarction (MI) in rats Methods Nine MI r...Objective To determine the relationship between remodeling and dysfunct ion of left ventricle (LV) and the expression of the angiotensin AT1 receptor mRNA after myocardial infarction (MI) in rats Methods Nine MI rats (Group A) and 8 shamoperated rats (Group B) were studied by both Doppler echocardiography and Dot blot using Digoxingeninlabel led cDNA probes Results Compared with Group B, Group A showed the increase in LV intern al diastolic diameter (087006?mm vs 066003?mm, respectively, P <001) and volume (073009?ml vs 051005?ml, P < 0 01) In addition, thinning of anterior wall, thickening of posterior wall, in cr easing of peak early filling velocity (peak E), decreasing of late filling veloc ity (peak A) and increasing of the E/A were demonstrated in MI rats 7 weeks aft er MI The levels of the cardiac angiotensin AT1 receptor mRNA in Group A we re higher than those of Group B (22fold) Conclusions Seven weeks after MI in rats, character of LV remodeling an d dysfunction were developed and the expression of cardiac angiotensin AT1 re ceptor mRNA was increased展开更多
文摘Using mice infected with coxsackie B-3 virus (CVB3) as a viral myocarditis model, we observed the inhibitory effect of Astragalus membranaceus (AM) on CVB3-RNA replication in myocardial tissue of mice by RNA-RNA in situ hybridization with negative-strand RNA Probes labelled with ￣(35)S and quantitative imaging analysis of positive signals. The mechanism of its effect on CVB3-RNA replication has been investigated by detection of beta-interferon (β-IFN) as well. Results showed that the copy numbers of CVB3-RNA as well as the histologic scores (necrosis) in myocardial tissues of infected-AM treated mice were significantly lower than those in infected and normal saline treated mice, suggesting that AM could inhibit the replication of CVB3-RVA,but its effect on CVB3-RNA replication had no correlation with induction of β-IFN.
文摘The effect of verapamil on Ca2+ influx across the myocardial plasma membrane and coxsackie virus B3 ( CVB3)-RNA replication in cultured neonatal rat heart cells infected with CVB3 was investigated. It was found that the Ca2+ influx could be inhibited significantly (P<O. 01) by verapamil (1 μmol/L) after infection of heart cells for 48h. However, when the cultured heart cells infected with CVB3 and treated with verapamil (Iμmol/L and 10 nmo/L) at the same time for 48h, the amounts of CVB3-RNA in myocytes were significantly higher than that in infected control group (P<O. 05). These phenomena suggest that the increase of Ca2+ influx of cultured heart cells infected with CVB3 could be inhibited by some calcium antagonists, e. g. verapamil at the early stage. On the other hand, verapamil might accelerate viral replication in myocardium. Thus, although verapamil could be beneficial for decreasing the secondary Ca2+ damages and improve the myocardial electric activity, it isn’t a sensible choice for therapy in early stage of virus infection with cardiac symptoms.
文摘Objective To determine the relationship between remodeling and dysfunct ion of left ventricle (LV) and the expression of the angiotensin AT1 receptor mRNA after myocardial infarction (MI) in rats Methods Nine MI rats (Group A) and 8 shamoperated rats (Group B) were studied by both Doppler echocardiography and Dot blot using Digoxingeninlabel led cDNA probes Results Compared with Group B, Group A showed the increase in LV intern al diastolic diameter (087006?mm vs 066003?mm, respectively, P <001) and volume (073009?ml vs 051005?ml, P < 0 01) In addition, thinning of anterior wall, thickening of posterior wall, in cr easing of peak early filling velocity (peak E), decreasing of late filling veloc ity (peak A) and increasing of the E/A were demonstrated in MI rats 7 weeks aft er MI The levels of the cardiac angiotensin AT1 receptor mRNA in Group A we re higher than those of Group B (22fold) Conclusions Seven weeks after MI in rats, character of LV remodeling an d dysfunction were developed and the expression of cardiac angiotensin AT1 re ceptor mRNA was increased
