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Posterior cataract opacification(PCO)is the epithelial-mesenchymal transformation(EMT)of residual lens epithelial cells(LECs)after cataract surgery, resulting in opaque scar which is one of the main complications of cataract surgery. A large amount of fibronectin(FN)produced by LECs after cataract surgery binds to a variety of cell surface receptors, matrix components and growth factors to regulate cell behavior. The purpose of this article is to review the literatures on the treatment of PCO targeting fibronectin and provide references for clinical treatment of PCO. In this paper, the research status of fibronectin in PCO in recent years is reviewed.
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<p><b>OBJECTIVE</b>To reveal the transmembrane signal pathway participating in regulating neuron functions of treating Alzheimer's disease (AD) by acupuncture.</p><p><b>METHODS</b>SAMP8 mice was used for AD animal model. The effect of acupuncture method for qi benefiting, blood regulating, health supporting, and root strengthening on the amount and varieties of transmembrane signal proteins from hippocampal lipid rafts in SAMP8 mice was detected using HPLC MS/MS proteomics method.</p><p><b>RESULTS</b>Compared with the control group, acupuncture increased 39 transmembrane signal proteins from hippocampal lipid rafts in SAMP8 mice, of them, 14 belonged to ionophorous protein, 8 to G protein, 8 to transmembrane signal receptor, and 9 to kinase protein. Totally 3 main cell signal pathways were involved, including G-protein-coupled receptors signal, enzyme linked receptor signal, and ion-channel mediated signal. Compared with the sham-acupuncture group, acupuncture resulted in significant increase of kinase signal protein amount. From the aspect of functions, they were dominant in regulating synapse functions relevant to cytoskeleton and secreting neurotransmitters.</p><p><b>CONCLUSION</b>The cell biological mechanism for treating AD by acupuncture might be achieved by improving synapse functions and promoting the secretion of neurotransmitters through transmembrane signal transduction, thus improving cognitive function of AD patients.</p>
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Animales , Femenino , Masculino , Ratones , Terapia por Acupuntura , Enfermedad de Alzheimer , Metabolismo , Modelos Animales de Enfermedad , Microdominios de Membrana , Metabolismo , Proteómica , Transducción de Señal , Espectrometría de Masas en TándemRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of Ganfukang (GFK) on connective tissue growth factor (CTGF) and focal adhesion kinase (FAK)/protein kinase B (PKB or Akt) signal pathway in a hepatic fibrosis rat model and to explore the underlying therapeutic molecular mechanisms of GFK.</p><p><b>METHODS</b>Fifty SD rats were randomly divided into five groups as follows: the control group, the model group (repeated subcutaneous injection of CCl4), and the three GFK treatment groups (31.25, 312.5, and 3125 mg/kg, intragastric administration). Reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemistry were used to examine the expression of CTGF, integrin α5, integrin β1, FAK/Akt signal pathway, cyclinD1, and collagen in the different-treated rats.</p><p><b>RESULTS</b>GFK attenuated the up-regulation of CTGF, integrin α5, and integrin β1 in hepatic fibrosis rats and suppressed both the phosphorylation of FAK and the phosphorylation of Akt simultaneously (P<0.01). At the same time, the expression of cyclinD1, collagen I, and collagen III was decreased by GFK significantly (P<0.01).</p><p><b>CONCLUSIONS</b>CTGF and FAK/Akt signal pathway were activated in the CCl4-induced hepatic fibrosis rats, which contribute to increased expression of cyclinD1 and collagen genes. The mechanisms of the anti-fibrosis activity of GFK may be due to its effects against CTGF and FAk/Akt signal pathway.</p>
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Animales , Femenino , Masculino , Colágeno , Genética , Metabolismo , Factor de Crecimiento del Tejido Conjuntivo , Genética , Metabolismo , Ciclina D1 , Genética , Metabolismo , Medicamentos Herbarios Chinos , Farmacología , Usos Terapéuticos , Proteína-Tirosina Quinasas de Adhesión Focal , Metabolismo , Regulación de la Expresión Génica , Integrina alfa5 , Genética , Metabolismo , Integrina beta1 , Genética , Metabolismo , Hígado , Patología , Cirrosis Hepática , Quimioterapia , Genética , Patología , Fosforilación , Proteínas Proto-Oncogénicas c-akt , Metabolismo , Ratas Sprague-Dawley , Transducción de SeñalRESUMEN
Objective To explore the influence of age-related changes in the cerebral blood vessels (cerebral blood flow,blood-brain barrier integrity,and level of glucose transporter [GLUT]) in cognitive ability of SAMP8 mouse models of AD. Methods Ten SAMP8 mice and 10 homologous anti-senescence accelerated mice R1 (SAMR1) were chosen in our study; spatial learning and memory abilities of these mice were assessed using Morris water maze; cerebral blood flow was determined by laser Doppler flowmeter; blood-brain barrier (BBB) permeability was examined by fluorescence spectrophotometer; and expressions of GLUT1 and GLUT3 were determined using Western blotting.Results The cognitive abilities of SAMP8 mice damaged apparently even at 4 months of age as compared with those of SAMR1 mice, showing rigid thinking pattern and slow learning process in their Morris water maze test. With increasing of age, much obvious decrement in cerebral blood flow and severe BBB leakage was observed in SAMP8 mice; moreover, alterations in GLUT1 and GLUT3 expressions in the cortex and hippocampus of SAMP8 mice were observed. The cerebral blood flow,BBB integrity,and expressions of GLUT1 and GLUT3 were significantly affected by age and strain,and closely associated with cognitive abilities. Conclusion The alterations in cerebral blood flow and energy failure induced by aging and vascular insults are the reasons for neuron dysfunction and cognitive impairment in mice models of AD.
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The acupuncture technique of tonifying qi, regulating blood and strengthening the primary source of human life is established on the base of the new pathology of dementia due to dysfunction of sanjiao by Prof. HAN Jing-xian. It is held that Tanzhong (CV 17), Zhongwan (CV 12), Qihai (CV 6), Xuehai (SP 10), Zusanli(ST 36) and Waiguan (TE 5) were the basic points for treatment of dementia. There are 3 characteristics of the point combination. Firstly, emphasis should be put on regulation of the stomach and the spleen so as to promote transportation, transformation and distribution; secondly, monarch, minister, assistant and guide points should be selected on the base of meridians, and more attention should be paid to the entity and connections among organs; and thirdly, treatment should be given according to physiological functions of the viscera.
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Humanos , Puntos de Acupuntura , Terapia por Acupuntura , Métodos , Circulación Sanguínea , Medicina Tradicional China , QiRESUMEN
The aim of this study was to evaluate the role of GATA4 in hypertrophy and survival functions of CT-1 in the heart, and to apply chemical inhibitor strategies to assess a possible interaction of signaling pathways involved in these processes. Expression of GATA4 was determined at the mRNA expression (polymerase chain reaction, PCR) and protein binding activity (electrophoretic mobility shift assays, EMSAs) levels. Myocardial apoptosis was detected using the in-situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Parthenolide (an inhibitor to STAT3) and U0126 (an MEK inhibitor to block ERK1/2) were used to assess a possible interaction of signaling pathways involved in the processes. The results showed that CT-1 had a significant role in the expression of GATA4 mRNA and binding activity of cardiomyocytes. The stronger expression of GATA4 mRNA stimulated by CT-1 was essentially mediated by STAT3, and was negatively regulated by ERK1/2. The intercross relationship between STAT3 and ERK1/2 might assist CT-1 in cardiac hypertrophy. At the same time, CT-1 had its effect on anti-apoptosis and survival of cardiac myocytes. During this process, GATA4 expression showed a negative relationship with myocardial apoptosis. Obviously, STAT3 cannot affect the anti-apoptotic process of CT-1, but obstruction of ERK signaling pathway can inhibit the CT-1 anti-apoptotic effect significantly. Our data suggest that CT-1 can affect the expression of GATA4 mRNA and the binding activity of cardiac myocytes. GATA4 plays an important role in the hypertrophic effect of CT-1, in which STAT3 plays a primary role. The regulation of CT-1 on the anti-apoptotic process is mediated partly by GATA4, and can be inhibited by obstructing the ERK signaling pathway.
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Apoptosis/fisiología , Cardiomegalia/metabolismo , Citocinas/metabolismo , Factor de Transcripción GATA4/metabolismo , Miocitos Cardíacos/metabolismo , Transducción de Señal/fisiología , Animales , Cardiomegalia/patología , Células Cultivadas , Ensayo de Cambio de Movilidad Electroforética , Inmunohistoquímica , Etiquetado Corte-Fin in Situ , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Miocitos Cardíacos/patología , ARN Mensajero/análisis , Ratas , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Transcripción STAT3/metabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of cardiotrophin-1 (CT-1) on the GATA4 expression and related signaling pathways (JAK-STAT3, ERK1/2 and PI3-K) in rat cardiomyocytes.</p><p><b>METHODS</b>Using semi-quantitative RT-PCR and EMSA, we measured the dose and time dependent effects of CT-1 on GATA4 mRNA and binding activity in cultured rat cardiomyocytes. Parthenolide (a STAT inhibitor), U-0126 (an ERK inhibitor) and LY-294002 (a PI3-K inhibitor) alone or in combination were added to the culture medium to assess the role of above signaling pathways in CT-1 mediated effects.</p><p><b>RESULTS</b>GATA4 mRNA expression significantly increased at 3 h post 0.1 nmol/L CT-1 exposure, peaked at 6 h and remained high till 24 h post exposure. The GATA4 binding activity began to increase at 10 min and peaked at 60 min and returned to baseline level 180 min. Six hours post CT-1 (0.01 nmol/L, 0.1 nmol/L, 1 nmol/L) exposure, the GATA4 mRNA expression increased in a dose-dependent manner. The GATA4 binding activity peaked with 0.1 nmol/L CT-1 and higher dose did not further increase the binding activity. U-0126 increased the GATA4 mRNA expression and enhanced the GATA4 binding activity and these effects could be partially attenuated with addition of Parthenolide. Parthenolide also prevented the increase of GATA4 mRNA and binding activity induced by CT-1. LY-294002 had no effects GATA4 mRNA and binding activity.</p><p><b>CONCLUSION</b>CT-1 increases the GATA4 mRNA expression and binding activity in rat cardiomyocytes via STAT3/ERK1/2 pathways and these effects are independent of PI3-K pathway.</p>
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Animales , Ratas , Línea Celular , Citocinas , Farmacología , Factor de Transcripción GATA4 , Genética , Miocitos Cardíacos , Metabolismo , ARN Mensajero , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Transcripción STAT3 , Farmacología , Transducción de SeñalRESUMEN
<p><b>OBJECTIVE</b>To explore the inhibitory effect and its mechanism of salviae miltiorrhizae and beta-aescinom natrium on the postburn acute lung injury in rats.</p><p><b>METHODS</b>Forty-five rats were randomly divided into sham control (C, n = 9), sodium chloride group (S, n = 9), salviae miltiorrhizae group (M, n = 9), beta-aescinom natrium group (A, n = 9), and combination group (MA, n = 9). The rats in M, A and MA groups were subjected to 30% TBSA III degree scald on the back, and all the rats were sacrificed at 24 PBH. The blood and pulmonary tissue samples were harvested from the rats at 24 PBH for the determination of leukocyte adhesiveness/aggregation (LAA) in peripheral blood, myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) contents, and the ratio of wet to dry weights (W/D) of lung tissue.</p><p><b>RESULTS</b>Compared with those in S group, the LAA in blood and the pulmonary tissue contents of MPO, MDA and W/D rate in M and A groups, and especially in MA group, were decreased significantly, but the SOD content in pulmonary tissue increased obviously in M and A groups, especially in MA group. Furthermore, blood LAA was positively correlated with pulmonary tissue MDA content.</p><p><b>CONCLUSION</b>Postburn intra-pulmonary agglutination and aggregation of PMNs and pulmonary injury by oxygen free radicals (OFRs) and their products could be inhibited by either Salviae Miltiorrhizae or beta-aescinom natrium. In addition, these agents could also increase the tissue content of antioxidant capacity and decrease pulmonary microvascular permeability and lung water content. The results indicated that all the agents used might be effective in prevention and treatment of postburn pulmonary injury, especially when used together.</p>