RESUMEN
Emodin has been reported to fulfill an important function in suppressing the vicious outcome of liver cancer. We aimed to elucidate the partial underlying molecular mechanism of emodin in inhibiting liver cancer, and we applied miRNA-sequence analysis and corresponding molecular functional experiments to find that the inhibitory effect of emodin on liver cancer was partly mediated by cellular autophagy through the miR-371a-5p/PTEN axis. The expression level of miR-371a-5p was down-regulated after emodin treatment in liver cancer cell lines (LCCLs). Restoring the expression level of miR-371a-5p attenuated the suppression of emodin on LCCLs. Additionally, we performed the prediction in relevant online databases and found that PTEN might functioned as a downstream target of miR-371a-5p to participate in the regulation on the above process. What's more, the detection of autophagy-related protein markers showed that LC3II was elevated accompanied by the decreased P62. The above results revealed that PTEN functioned as a key target to regulate the autophagy in the process where emodin inhibited the malignant outcome of LCCLs via miR-371a-5p, which further provided a theoretical basis for the application of traditional Chinese medicine (TCM) on clinical tumors.
Asunto(s)
Emodina , Neoplasias Hepáticas , MicroARNs , Autofagia/fisiología , Proliferación Celular/fisiología , Emodina/farmacología , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/genética , MicroARNs/metabolismo , Fosfohidrolasa PTEN/genética , Fosfohidrolasa PTEN/metabolismoRESUMEN
Neurodegenerative diseases are frequently associated with the loss of synapses and neurons. Senegenin, extracted from the Chinese herb Polygala tenuifolia Willd, was previously found to promote neurite outgrowth and neuronal survival in primary cultured rat cortical neurons. The aim of the present study was to investigate the underlying mechanisms of senegenin-induced neurotrophic effects on rat cortical neurons. Primary cortical rat neurons were treated with various pharmacological antagonists and with or without senegenin, and subjected to MTT and western blot analysis to explore the effects of senegenin on cell survival as well as the activation of signaling pathways. Neurite outgrowth and neuronal survival induced by senegenin were significantly inhibited by A2A receptor antagonist ZM241385 and specific phosphoinositide-3 kinase (PI3K) inhibitor LY294002, but not by tropomyosin receptor kinase A receptor inhibitor K252a, mitogen-activated protein kinase kinase inhibitor PD98059 or protein kinase C inhibitor GÖ6976. Furthermore, senegenin enhanced the phosphorylation of Akt, which was blocked by LY294002. The present study revealed that the PI3K/Akt signaling pathway may be involved in the neurotrophic effects of senegenin.
Asunto(s)
Medicamentos Herbarios Chinos/administración & dosificación , Enfermedades Neurodegenerativas/tratamiento farmacológico , Neuronas/efectos de los fármacos , Fosfatidilinositol 3-Quinasas/biosíntesis , Proteínas Proto-Oncogénicas c-akt/biosíntesis , Animales , Supervivencia Celular/efectos de los fármacos , Cromonas/administración & dosificación , Medicamentos Herbarios Chinos/química , Humanos , Morfolinas/administración & dosificación , Neuritas/efectos de los fármacos , Neuritas/patología , Enfermedades Neurodegenerativas/genética , Enfermedades Neurodegenerativas/patología , Neuronas/patología , Fosfatidilinositol 3-Quinasas/genética , Polygala/química , Cultivo Primario de Células , Proteínas Proto-Oncogénicas c-akt/genética , Ratas , Transducción de Señal/efectos de los fármacos , Triazinas/administración & dosificación , Triazoles/administración & dosificaciónRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of moxibustion at Sanyinjiao (SP 6) for uterine contraction pain in labor, and evaluate the safety of the parturient and newborn.</p><p><b>METHODS</b>One hundred and seventy-four cases of singleton pregnancy and cephalic presentation primipara were single blinded and randomly divided into three groups: observation group (59 cases), placebo treated group (57 cases) and blank group (58 cases). The observation group was treated with moxibustion at Sanyinjiao (SP 6) for 30 min when the uterus cervix openning at 3 cm, the placebo treated group was treated with moxibustion at no acupoint for 30 min and the blank group was treated with routine labor nursing, the uterine contraction pain and the safety of the mother and infant were compared among three groups.</p><p><b>RESULTS</b>1) The uterine contraction pain was tested by Visual Analogue Scale (VAS): the scores of VAS in the observation group were obviously decreased after 15 min and 30 min of moxibustion (both P<0.05), there were no obvious changes of the VAS scores in placebo treated group and the blank group, the scores of VAS in observation group decreased much more obviously than those in the other two groups (all P<0.05); 2) Midwife rating of the uterine contraction pain: after 30 min of moxibustion, the effective rate of labor analgesia was 69.5% (41/59) in observation group, which was higher than that of 45.6% (26/57) in placebo treated group and 43.1% (25/58) in blank group, with significant differences between them (both P<0.05); 3) The postpartum hemorrhage amount of the observation group was obviously lower than those of placebo treated group and blank group (both P<0.05); 4) The Apgar score of newborn was higher in observation group and placebo treated group than that of blank group (both P<0.05).</p><p><b>CONCLUSION</b>Moxibustion at Sanyinjiao (SP 6) can relieve the uterine contraction pain, and has no side effect to mother and infant, it is one of the safe, effective and simple non-drug analgesia methods.</p>
Asunto(s)
Adulto , Femenino , Humanos , Embarazo , Adulto Joven , Puntos de Acupuntura , Dolor de Parto , Terapéutica , Trabajo de Parto , Moxibustión , Resultado del Tratamiento , Contracción UterinaRESUMEN
OBJECTIVE: To investigate the value of conventional magnetic resonance imaging (MRI) and diffusion weighed imaging (DWI) in the differentiation of hypoxic-ischemic encephalopathy (HIE) and acute bilirubin encephalopathy in neonates. METHODS: The MRI findings along with DWI characteristics in 15 neonates with HIE involving basal ganglia and in 18 neonates with acute bilirubin encephalopathy between November 2006 and June 2008 were retrospectively reviewed. RESULTS: On T1WI, only 5 patients presented hyperintensity in the globus pallidus in the HIE group, but 16 in the acute bilirubin encephalopathy group (p<0.01). Nine patients in the HIE group showed hyperintensity in the putamen, but the hyperintensity in the putamen was not found in the acute bilirubin encephalopathy group. The frequency of hyperintensity in the subthalamus in the acute bilirubin encephalopathy group (55.6%) was significantly higher than that in the HIE group (13.3%) (p<0.05). Eight patients in the HIE group showed abnormal signals in the other regions on T1WI, but only two patients in the acute bilirubin encephalopathy group (p<0.05). On DWI, 7 out of 11 patients with HIE presented hyperintensity in the basal ganglia, while all 10 patients of the acute bilirubin encephalopathy group presented normal in the basal ganglia. CONCLUSIONS: Conventional MRI along with DWI is useful in differentiating HIE from acute bilirubin encephalopathy in neonates.
Asunto(s)
Hipoxia-Isquemia Encefálica/diagnóstico , Kernicterus/diagnóstico , Imagen por Resonancia Magnética/métodos , Enfermedad Aguda , Encéfalo/patología , Diagnóstico Diferencial , Imagen de Difusión por Resonancia Magnética , Humanos , Hipoxia-Isquemia Encefálica/patología , Recién Nacido , Kernicterus/patología , Putamen/patología , Tálamo/patologíaRESUMEN
Manganese superoxide dismutase (MnSOD) is the only primary antioxidant enzyme in mitochondria that scavenges superoxide radicals. Overexpressing MnSOD in cancer cells by cDNA transfection suppresses tumor formation and reverses malignant growth. In this study, we examined the effect of recombinant human manganese superoxide dismutase (rhMnSOD) alone and in combination with adriamycin (ADR) against solid tumors of sarcoma 180 in Institute of Cancer Research (ICR) mice. Administration of rhMnSOD alone and in combination with ADR significantly inhibited tumor growth in a dose-dependent manner. The use of rhMnSOD in combination with ADR enhanced ADR's anti-tumor potency without increasing toxicity. Histopathological examination provided evidence of the anti-tumor effect. In addition, we found lymphocyte infiltration of the tumors, with an increase in both CD4- and CD8-positive cells in the treated tumors. The expression of CD4 and CD8 was up-regulated with increasing dose of rhMnSOD, and the combination treatment with ADR further enhanced this up-regulation. Collectively, these data indicate that rhMnSOD may exhibit an anti-tumor effect by stimulating the immune system and promoting the recruitment of lymphocytes into the tumor to kill tumor cells. Thus MnSOD may constitute a potential new therapeutic agent to be exploited as an adjuvant in cancer therapy.
Asunto(s)
Protocolos de Quimioterapia Combinada Antineoplásica , Doxorrubicina/uso terapéutico , Proteínas Recombinantes/uso terapéutico , Sarcoma 180/tratamiento farmacológico , Superóxido Dismutasa/uso terapéutico , Animales , Linfocitos T CD4-Positivos/inmunología , Linfocitos T CD8-positivos/inmunología , Modelos Animales de Enfermedad , Humanos , Linfocitos Infiltrantes de Tumor , Ratones , Sarcoma 180/inmunología , Sarcoma 180/patologíaRESUMEN
OBJECTIVE: To observe the effects of resveratrol on proliferation of human hepatocellular carcinoma cell line SMMC-7721 cells and expression of matrix metalloproteinase-9 (MMP-9) in vitro. METHODS: SMMC-7721 cells were treated with different concentrations of resveratrol for 24, 48 and 72 h, respectively. The effect of resveratrol on proliferation of SMMC-7721 cells was assessed with methyl thiazolyl tetrazolium (MTT). The expression of MMP-9 mRNA was determined by reverse transcription polymerase chain reaction (RT-PCR). MMP-9 protein was identified by Western blot analysis. RESULTS: Resveratrol could inhibit the proliferation of SMMC-7721 cells with dose- and time-dependent effects. Moreover, both MMP-9 mRNA expression and MMP-9 protein production were markedly reduced after resveratrol treatment. CONCLUSION: Resveratrol can inhibit the proliferation of SMMC-7721 cells and down-regulate MMP-9 expression. It is presumed that resveratrol may suppress the invasion and metastasis of hepatocellular carcinoma.
Asunto(s)
Carcinoma Hepatocelular/enzimología , Neoplasias Hepáticas/enzimología , Metaloproteinasa 9 de la Matriz/metabolismo , Estilbenos/farmacología , Antineoplásicos Fitogénicos/farmacología , Carcinoma Hepatocelular/patología , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Regulación hacia Abajo/efectos de los fármacos , Humanos , Neoplasias Hepáticas/patología , Metaloproteinasa 9 de la Matriz/genética , ARN Mensajero/genética , ARN Mensajero/metabolismo , Resveratrol , Células Tumorales CultivadasRESUMEN
OBJECTIVE: To observe the efficacy of modified acupotome combined with blocking therapy in patients with carpal tunnel syndrome (CTS). METHODS: Fifty-five patients with CTS were divided into three groups, which were modified acupotome group including 26 CTS patients with 28 lesions treated by modified acupotome combined with blocking therapy, traditional acupotome group including 14 CTS patients with 16 lesions treated by traditional acupotome combined with blocking therapy, and blocking therapy group including 15 CTS patients with 15 lesions only treated by local blocking. The treatment outcome and one-year recurrence rate were observed. RESULTS: The response rate and one-year recurrence rate after operation in the modified acupotome group were 85.7% (24/28) and 20.8% (5/24) respectively, which had no significant differences as compared with 81.3% (13/16) and 38.5% (5/13) in the traditional acupotome group. The response rate and one-year recurrence rate after operation in the above two groups were both improved significantly as compared with those in the blocking therapy group which were 46.7% (7/15) and 85.7% (6/7) respectively. There were no acupotome-related adverse effects and injuries observed in the modified acupotome group. CONCLUSION: The modified acupotome is a considerable treatment method for CTS with respect to its simple manipulation and high effectiveness.
Asunto(s)
Terapia por Acupuntura/métodos , Síndrome del Túnel Carpiano/terapia , Descompresión Quirúrgica/métodos , Bloqueo Nervioso , Adulto , Terapia Combinada , Descompresión Quirúrgica/instrumentación , Femenino , Humanos , Masculino , Persona de Mediana Edad , Bloqueo Nervioso/métodosRESUMEN
After spinal cord injury, enzymatic digestion of chondroitin sulfate proteoglycans promotes axonal regeneration of central nervous system neurons across the lesion scar. We examined whether chondroitinase ABC (ChABC) promotes the axonal regeneration of rubrospinal tract (RST) neurons following injury to the spinal cord. The effect of a GSK-3beta inhibitor, lithium chloride (LiCl), on the regeneration of axotomized RST neurons was also assessed. Adult rats received a unilateral hemisection at the seventh cervical spinal cord segment (C7). Four weeks after different treatments, regeneration of RST axons across the lesion scar was examined by injection of Fluoro-Gold at spinal segment T2, and locomotor recovery was studied by a test of forelimb usage. Injured RST axons did not regenerate spontaneously after spinal cord injury, and intraperitoneal injection of LiCl alone did not promote the regeneration of RST axons. Administration of ChABC at the lesion site enhanced the regeneration of RST axons by 20%. Combined treatment of LiCl together with ChABC significantly increased the regeneration of RST axons to 42%. Animals receiving combined treatment used both forelimbs together more often than animals that received sham or single treatment. Immunoblotting and immunohistochemical analysis revealed that LiCl induced the expression of inactive GSK-3beta as well as the upregulation of Bcl-2 in injured RST neurons. These results indicate that in vivo, LiCl inhibits GSK-3beta and reinforces the regeneration-promoting function of ChABC through a Bcl-2-dependent mechanism. Combined use of LiCl together with ChABC could be a novel treatment for spinal cord injury.