RESUMEN
Bovine viral diarrhea virus can cause acute disease in livestock, leading to economic losses. We show that Prostaglandin A1 inhibits bovine viral diarrhea virus replication in Madin-Darby bovine kidney cells (94% inhibition using 5 µg/mL). Light and electron microscopy of infected cells shows that Prostaglandin A1 also prevents virus-induced vacuolization, but at higher concentrations (10 µg/mL).(AU)
Asunto(s)
Animales , Bovinos , Virus de la Diarrea Viral Bovina , Prostaglandinas A/uso terapéutico , Replicación Viral , Vacuolas , Microscopía Electrónica/veterinariaRESUMEN
Atherosclerosis is a multifactorial inflammatory disease of blood vessels which decimates one in every three people in industrialized world. Despite the important newest clinical approaches, currently available strategies (e.g. nutritional, pharmacological and surgical) may only restrain the worsening of vascular disease. Since antiproliferative cyclopentenone prostaglandins (CP-PGs) are powerful anti-inflammatory agents, we developed a negatively charged liposome-based pharmaceutical formulation (LipoCardium) that specifically direct CP-PGs towards the injured arterial wall cells of atherosclerotic mice. In the blood stream, LipoCardium delivers its CP-PG contents only into activated arterial wall lining cells due to the presence of antibodies raised against vascular cell adhesion molecule-1 (VCAM-1), which is strongly expressed upon inflammation by endothelial cells and macrophage-foam cells as well. After 4 months in a high-lipid diet, all low-density lipoprotein receptor-deficient adult control mice died from myocardium infarction or stroke in less than 2 weeks, whereas LipoCardium-treated (2 weeks) animals (still under high-lipid diet) completely recovered from vascular injuries. In vitro studies using macrophage-foam cells suggested a tetravalent pattern for LipoCardium action: anti-inflammatory, antiproliferative (and pro-apoptotic only to foam cells), antilipogenic and cytoprotector (via heat-shock protein induction). These astonishing cellular effects were accompanied by a marked reduction in arterial wall thickness, neointimal hyperplasia and lipid accumulation, while guaranteed lifespan to be extended to the elderly age. Our findings suggest that LipoCardium may be safely tested in humans in a near future and may have conceptual implications in atherosclerosis therapy.
Asunto(s)
Aterosclerosis/tratamiento farmacológico , Metabolismo de los Lípidos/efectos de los fármacos , Prostaglandinas/farmacología , Prostaglandinas/uso terapéutico , Animales , Aterosclerosis/fisiopatología , Ciclopentanos/farmacología , Modelos Animales de Enfermedad , Estudios de Factibilidad , Liposomas , Macrófagos/efectos de los fármacos , Masculino , Ratones , Prostaglandinas A/farmacología , Prostaglandinas A/uso terapéutico , Ratas , Ratas WistarRESUMEN
The effect of prostaglandins (PGA1 and PGB2) on the replication of Mayaro virus was studied in Vero cells. PGA1 and PGB2 antiviral activity was found to be dose-dependent. However, while 10 µg/ml PGB2 inhibited virus yield by 60 percent, at the same dose PGA1 suppressed virus replication by more than 90 percent. SDS-PAGE analysis of [35S]-methionine-labelled proteins showed that PGA1 did not alter cellular protein synthesis. In infected cells, PGA1 slightly inhibited the synthesis of protein C, while drastically inhibiting the synthesis of glycoproteins E1 and E2
Asunto(s)
Animales , Alphavirus/fisiología , Prostaglandinas A/farmacología , Prostaglandinas B/farmacología , Células Vero/efectos de los fármacos , Replicación Viral/efectos de los fármacos , Infecciones por Alphavirus/tratamiento farmacológico , Alphavirus/efectos de los fármacos , Alphavirus/crecimiento & desarrollo , Glicoproteínas/biosíntesis , Metionina/análisis , Prostaglandinas A/metabolismo , Prostaglandinas A/uso terapéutico , Prostaglandinas B/metabolismo , Prostaglandinas B/uso terapéutico , Proteína C/biosíntesisRESUMEN
Prostaglandins (Pgs) have been shown to inhibit the replication of several DNA and RNA viruses. Here we report the effect of prostaglandin (PgA1) on the multiplication of a positive strand RNA virus, Classical Swine Fever Virus (CSFV) in PK15 cells. PgA1 was found to inhibit the multiplication of CSFV. At a concentration of 5 micrograms/ml, which was nontoxic to the cells, PgA1 inhibitis virus production in 99%. In PgA1 treated cells the size and number of characteristic Classical Swine Fever focus decreased in amount.
Asunto(s)
Virus de la Fiebre Porcina Clásica/fisiología , Peste Porcina Clásica/tratamiento farmacológico , Prostaglandinas A/farmacología , Replicación Viral/efectos de los fármacos , Animales , Virus de la Fiebre Porcina Clásica/efectos de los fármacos , ADN Viral/efectos de los fármacos , Proteínas de Choque Térmico/biosíntesis , Prostaglandinas A/uso terapéutico , ARN Viral/efectos de los fármacos , PorcinosRESUMEN
The effect of prostaglandins (PGA1 and PGB2) on the replication of Mayaro virus was studied in Vero cells. PGA1 and PGB2 antiviral activity was found to be dose-dependent. However, while 10 micrograms/ml PGB2 inhibited virus yield by 60%, at the same dose PGA1 suppressed virus replication by more than 90%. SDS-PAGE analysis of [35S]-methionine-labelled proteins showed that PGA1 did not alter cellular protein synthesis. In infected cells, PGA1 slightly inhibited the synthesis of protein C, while drastically inhibiting the synthesis of glycoproteins E1 and E2.