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Mol Med Rep ; 12(3): 3557-3562, 2015 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-25998024


Ginsenoside Rg3 is one of the main constituents isolated from Panax ginseng, and exhibits cytotoxic effects against cancer cells. The present study aimed to investigate the effects of ginsenoside Rg3 on human multiple myeloma cells, and determine the underlying molecular mechanisms. The cells were exposed to ginsenoside Rg3 at various concentrations (0­80 µM) for 48 h. A subsequent cell proliferation assay demonstrated that treatment with ginsenoside Rg3 resulted in a dose­dependent inhibition of the proliferation of U266 and RPMI8226 cells. Furthermore, exposure to ginsenoside Rg3 led to a marked increase in the rate of apoptosis in the U266 cells, coupled with increased caspase­3 activity. The ginsenoside Rg3­treated cells also exhibited an elevation in the expression of B­cell lymphoma 2­associated X protein (Bax), a pro­apoptotic protein. Notably, knockdown of Bax protected the U266 cells from Rg3­induced apoptosis. Overall, these findings suggested that ginsenoside Rg3 induced apoptosis in multiple myeloma cells, at least partially, through upregulation of the expression of Bax.

Antineoplásicos Fitogénicos/farmacología , Apoptosis/efectos de los fármacos , Ginsenósidos/farmacología , Mieloma Múltiple/tratamiento farmacológico , Proteína X Asociada a bcl-2/metabolismo , Antineoplásicos Fitogénicos/química , Línea Celular Tumoral , Ginsenósidos/química , Humanos , Mieloma Múltiple/metabolismo , Mieloma Múltiple/patología , Panax/química
Eur J Med Res ; 18: 16, 2013 Jun 05.
Artículo en Inglés | MEDLINE | ID: mdl-23738715


BACKGROUND: Recent studies haveshown that ginsenoside Rg1, extracted from the dry roots of Panax notoginseng as a traditional Asian medicine, plays an anti-fibrosis role in myocardial remodeling. However, the mechanism still remains unclear. In the present study, we investigate the effect of ginsenoside Rg1on the collagenic remodeling of myocardium in chronic thromboembolic pulmonary hypertension (CTEPH), and its potential mechanism. METHODS: A rat model of CTEPH was established by injecting thrombi through the jugular vein wice in2 weeks. Four weeks later, four groups (Group A: normal rats + normal saline; Group B: normal rats + Rg1; Group C: CTEPH model + normal saline; Group D: CTEPH model + Rg1) were established. Normal saline and Rg1 were administrated by intraperitoneal injection. Ineach group, we measured the hemodynamic parameters, as well as the right ventricle to left ventricle (RV/LV) thickness ratio. Myocardial tissue sections of the RV were stained by hematoxylin-eosin +gentian violet and the morphological characteristics were observed by light microscopy. The matrix metalloproteinases (MMP) -2 and -9 were detected by the western blot. RESULTS: Compared with Group A and Group B, the right ventricular systolic pressure was significantly increased in Group C and significantly decreased in Group D. Compared with Group A and Group B, the RV/LV thickness ratio of the rats was significantly higher in Group C and Group D. There was significant fibrosis with collagen in Group C compared with Group A and Group B, and less significant changes in Group D were observed compared with those in Group C. The expression of MMP-2 and MMP-9 exhibited a significant decrease in Group C and was also significantly decreased in Group D compared withGroup A and Group B. Also, a negative linear relationship was shown between collagen-I and the expression of MMP-2 and MMP-9. CONCLUSIONS: Our animal study showed that ginsenoside Rg1 positively affects myocardial remodeling and pulmonary hemodynamics in CTEPH. Upregulation of the expression of MMP-2 and MMP-9 could explain the beneficial effects of ginsenoside Rg1 in CTEPH.

Regulación de la Expresión Génica/efectos de los fármacos , Ginsenósidos/administración & dosificación , Hipertensión Pulmonar/tratamiento farmacológico , Embolia Pulmonar/tratamiento farmacológico , Animales , Modelos Animales de Enfermedad , Ginsenósidos/química , Ventrículos Cardíacos/efectos de los fármacos , Ventrículos Cardíacos/fisiopatología , Humanos , Hipertensión Pulmonar/fisiopatología , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/metabolismo , Panax notoginseng/química , Embolia Pulmonar/fisiopatología , Ratas , Remodelación Ventricular/efectos de los fármacos
PLoS One ; 8(2): e56407, 2013.
Artículo en Inglés | MEDLINE | ID: mdl-23437127


BACKGROUND: Nuclear factor-κB (NF-κB) is a central transcriptional factor and a pleiotropic regulator of many genes involved in acute lung injury. Andrographolide is found in the plant of Andrographis paniculata and widely used in Traditional Chinese Medicine, exhibiting potently anti-inflammatory property by inhibiting NF-κB activity. The purpose of our investigation was designed to reveal the effect of andrographolide on various aspects of LPS induced inflammation in vivo and in vitro. METHODS AND RESULTS: In vivo, BALB/C mice were subjected to LPS injection with or without andrographolide treatments to induce ALI model. In vitro, MLE-12 cells were stimulated with LPS in the presence and absence of andrographolide. In vivo, pulmonary inflammation, pulmonary edema, ultrastructure changes of type II alveolar epithelial cells, MPO activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1ß in BALF, along with the expression of VCAM-1 and VEGF were dose-dependently attenuated by andrographolide. Meanwhile, in vitro, the expression of VCAM-1 and VEGF was also reduced by andrographolide. Moreover, our data showed that andrographolide significantly inhibited the ratios of phospho-IKKß/total IKKß, phospho-IκBα/total IκBα and phospho-NF-κB p65/total NF-κB p65, and NF-κB p65 DNA binding activities, both in vivo and in vitro. CONCLUSIONS: These results indicate that andrographolide dose-dependently suppressed the severity of LPS-induced ALI, more likely by virtue of andrographolide-mediated NF-κB inhibition at the level of IKKß activation. These results suggest andrographolide may be considered as an effective and safe drug for the potential treatment of ALI.

Lesión Pulmonar Aguda/tratamiento farmacológico , Lesión Pulmonar Aguda/metabolismo , Diterpenos/uso terapéutico , FN-kappa B/metabolismo , Sustancias Protectoras/uso terapéutico , Lesión Pulmonar Aguda/genética , Lesión Pulmonar Aguda/patología , Células Epiteliales Alveolares/patología , Células Epiteliales Alveolares/ultraestructura , Animales , Líquido del Lavado Bronquioalveolar , Recuento de Células , Supervivencia Celular/efectos de los fármacos , Supervivencia Celular/genética , Citocinas/metabolismo , ADN/metabolismo , Diterpenos/farmacología , Regulación hacia Abajo/efectos de los fármacos , Regulación de la Expresión Génica/efectos de los fármacos , Lipopolisacáridos , Masculino , Ratones , Ratones Endogámicos BALB C , Peroxidasa/metabolismo , Neumonía/complicaciones , Neumonía/tratamiento farmacológico , Neumonía/genética , Neumonía/patología , Sustancias Protectoras/farmacología , Unión Proteica/efectos de los fármacos , Unión Proteica/genética , Edema Pulmonar/complicaciones , Edema Pulmonar/tratamiento farmacológico , Edema Pulmonar/genética , Edema Pulmonar/patología , Factor de Transcripción ReIA/metabolismo , Molécula 1 de Adhesión Celular Vascular/genética , Molécula 1 de Adhesión Celular Vascular/metabolismo , Factor A de Crecimiento Endotelial Vascular/genética , Factor A de Crecimiento Endotelial Vascular/metabolismo