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1.
Acta Pharmacol Sin ; 40(5): 589-598, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30030529

RESUMO

High-mobility group box 1 (HMGB1) exhibits various functions according to its subcellular location, which is finely conditioned by diverse post-translational modifications, such as acetylation. The nuclear HMGB1 may prevent from cardiac hypertrophy, whereas its exogenous protein is proven to induce hypertrophic response. This present study sought to investigate the regulatory relationships between poly(ADP-ribose) polymerase 1 (PARP1) and HMGB1 in the process of pathological myocardial hypertrophy. Primary-cultured neonatal rat cardiomyocytes (NRCMs) were respectively incubated with three cardiac hypertrophic stimulants, including angiotensin II (Ang II), phenylephrine (PE), and isoproterenol (ISO), and cell surface area and the mRNA expression of hypertrophic biomarkers were measured. the catalytic activity of PARP1 was remarkably enhanced, meanwhile HMGB1 excluded from the nucleus. PARP1 overexpression by infecting with adenovirus PARP1 (Ad-PARP1) promoted the nuclear export of HMGB1, facilitated its secretion outside the cell, aggravated cardiomyocyte hypertrophy, which could be alleviated by HMGB1 overexpression. PE treatment led to the similar results, while that effect was widely depressed by PARP1 silencing or its specific inhibitor AG14361. Moreover, SD rats were intraperitoneally injected with 3-aminobenzamide (3AB, 20 mg/kg every day, a well-established PARP1 inhibitor) 7 days after abdominal aortic constriction (AAC) surgery for 6 weeks, echocardiography and morphometry of the hearts were measured. Pre-treatment of 3AB relieved AAC-caused the translocation of nuclear HMGB1 protein, cardiac hypertrophy, and heart dysfunction. Our research offers a novel evidence that PARP1 combines with HMGB1 and accelerates its translocation from nucleus to cytoplasm, and the course finally causes cardiac hypertrophy.


Assuntos
Cardiomegalia/etiologia , Núcleo Celular/metabolismo , Proteína HMGB1/metabolismo , Poli(ADP-Ribose) Polimerase-1/metabolismo , Transporte Ativo do Núcleo Celular/efeitos dos fármacos , Angiotensina II/farmacologia , Animais , Isoproterenol/farmacologia , Masculino , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Fenilefrina/farmacologia , Ratos Sprague-Dawley
2.
Acta Pharmacol Sin ; 39(12): 1837-1846, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29991711

RESUMO

Vascular endothelial cell senescence is a leading cause of age-associated and vascular diseases. Mammalian target of rapamycin complex 2 (mTORC2) is a conserved serine/threonine (Ser/Thr) protein kinase that plays an important regulatory role in various cellular processes. However, its impact on endothelial senescence remains controversial. In this study we investigated the role and molecular mechanisms of mTORC2 in endothelial senescence. A replicative senescence model and H2O2-induced premature senescence model were established in primary cultured human umbilical vein endothelial cells (HUVECs). In these senescence models, the formation and activation of mTORC2 were significantly increased, evidenced by the increases in binding of Rictor (the essential component of mTORC2) to mTOR, phosphorylation of mTOR at Ser2481 and phosphorylation of Akt (the effector of mTORC2) at Ser473. Knockdown of Rictor or treatment with the Akt inhibitor MK-2206 attenuated senescence-associated ß-galactosidase (ß-gal) staining and expression of p53 and p21 proteins in the senescent endothelial cells, suggesting that mTORC2/Akt facilitates endothelial senescence. The effect of mTORC2/Akt on endothelial senescence was due to suppression of nuclear factor erythroid 2-related factor 2 (Nrf2) at the transcriptional level, since knockdown of Rictor reversed the reduction of Nrf2 mRNA expression in endothelial senescence. Furthermore, mTORC2 suppressed the expression of Nrf2 via the Akt/GSK-3ß/C/EBPα signaling pathway. These results suggest that the mTORC2/Akt/GSK-3ß/C/EBPα/Nrf2 signaling pathway is involved in both replicative and inducible endothelial senescence. The deleterious role of mTORC2 in endothelial cell senescence suggests therapeutic strategies (targeting mTORC2) for aging-associated diseases and vascular diseases.


Assuntos
Senescência Celular/fisiologia , Células Endoteliais/fisiologia , Alvo Mecanístico do Complexo 2 de Rapamicina/fisiologia , Proteína alfa Estimuladora de Ligação a CCAAT/metabolismo , Glicogênio Sintase Quinase 3 beta/metabolismo , Células Endoteliais da Veia Umbilical Humana , Humanos , Fator 2 Relacionado a NF-E2/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/fisiologia
3.
Acta Pharmacol Sin ; 39(5): 802-824, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29698387

RESUMO

Salvia miltiorrhiza Burge (Danshen) is an eminent medicinal herb that possesses broad cardiovascular and cerebrovascular protective actions and has been used in Asian countries for many centuries. Accumulating evidence suggests that Danshen and its components prevent vascular diseases, in particular, atherosclerosis and cardiac diseases, including myocardial infarction, myocardial ischemia/reperfusion injury, arrhythmia, cardiac hypertrophy and cardiac fibrosis. The published literature indicates that lipophilic constituents (tanshinone I, tanshinone IIa, tanshinone IIb, cryptotanshinone, dihydrotanshinone, etc) as well as hydrophilic constituents (danshensu, salvianolic acid A and B, protocatechuic aldehyde, etc) contribute to the cardiovascular protective actions of Danshen, suggesting a potential synergism among these constituents. Herein, we provide a systematic up-to-date review on the cardiovascular actions and therapeutic potential of major pharmacologically active constituents of Danshen. These bioactive compounds will serve as excellent drug candidates in small-molecule cardiovascular drug discovery. This article also provides a scientific rationale for understanding the traditional use of Danshen in cardiovascular therapeutics.


Assuntos
Cardiotônicos/uso terapêutico , Doenças Cardiovasculares/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Animais , Doenças Cardiovasculares/fisiopatologia , Sinergismo Farmacológico , Células Endoteliais/efeitos dos fármacos , Fibrinolíticos/uso terapêutico , Humanos , Músculo Liso Vascular/efeitos dos fármacos , Miócitos de Músculo Liso/efeitos dos fármacos , Salvia miltiorrhiza
4.
Acta Pharmacol Sin ; 38(9): 1257-1268, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28649129

RESUMO

Phosphodiesterase-9A (PDE9A) expression is upregulated during cardiac hypertrophy and heart failure. Accumulating evidence suggests that PDE9A might be a promising therapeutic target for heart diseases. The present study sought to investigate the effects and underlying mechanisms of C33(S), a novel selective PDE9A inhibitor, on cardiac hypertrophy in vitro and in vivo. Treatment of neonatal rat cardiomyocytes (NRCMs) with PE (100 µmol/L) or ISO (1 µmol/L) induced cardiac hypertrophy characterized by significantly increased cell surface areas and increased expression of fetal genes (ANF and BNP). Furthermore, PE or ISO significantly increased the expression of PDE9A in the cells; whereas knockdown of PDE9A significantly alleviated PE-induced hypertrophic responses. Moreover, pretreatment with PDE9A inhibitor C33(S) (50 and 500 nmol/L) or PF-7943 (2 µmol/L) also alleviated the cardiac hypertrophic responses in PE-treated NRCMs. Abdominal aortic constriction (AAC)-induced cardiac hypertrophy and ISO-induced heart failure were established in SD rats. In ISO-treated rats, oral administration of C33(S) (9, 3, and 1 mg·kg-1·d-1, for 3 consecutive weeks) significantly increased fractional shortening (43.55%±3.98%, 54.79%±1.95%, 43.98%±7.96% vs 32.18%±6.28%), ejection fraction (72.97%±4.64%, 84.29%±1.56%, 73.41%±9.37% vs 49.17%±4.20%) and cardiac output (60.01±9.11, 69.40±11.63, 58.08±8.47 mL/min vs 48.97±2.11 mL/min) but decreased the left ventricular internal diameter, suggesting that the transition to heart failure was postponed by C33(S). We further revealed that C33(S) significantly elevated intracellular cGMP levels, phosphorylation of phospholamban (PLB) and expression of SERCA2a in PE-treated NRCMs in vitro and in ISO-induced heart failure model in vivo. Our results demonstrate that C33(S) effectively protects against cardiac hypertrophy and postpones the transition to heart failure, suggesting that it is a promising agent in the treatment of cardiac diseases.


Assuntos
3',5'-AMP Cíclico Fosfodiesterases/antagonistas & inibidores , Cardiomegalia/tratamento farmacológico , GMP Cíclico/metabolismo , Inibidores Enzimáticos/farmacologia , Pirazóis/farmacologia , Pirimidinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos , 3',5'-AMP Cíclico Fosfodiesterases/metabolismo , Animais , Cardiomegalia/metabolismo , Cardiomegalia/patologia , Células Cultivadas , Relação Dose-Resposta a Droga , Inibidores Enzimáticos/administração & dosagem , Inibidores Enzimáticos/química , Masculino , Miócitos Cardíacos/efeitos dos fármacos , Pirazóis/administração & dosagem , Pirazóis/química , Pirimidinas/administração & dosagem , Pirimidinas/química , Ratos , Ratos Sprague-Dawley , Relação Estrutura-Atividade
5.
Acta Pharmacol Sin ; 38(5): 638-650, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28239158

RESUMO

We previously identified AG-690/11026014 (6014) as a novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor that effectively prevented angiotensin II (Ang II)-induced cardiomyocyte hypertrophy. In the present study, we reported a new synthesis route for 6014, and investigated its protective effects on Ang II-induced cardiac remodeling and cardiac dysfunction and the underlying mechanisms in mice. We designed a new synthesis route to obtain a sufficient quantity of 6014 for this in vivo study. C57BL/6J mice were infused with Ang II and treated with 6014 (10, 30, 90 mg·kg-1·d-1, ig) for 4 weeks. Then two-dimensional echocardiography was performed to assess the cardiac function and structure. Histological changes of the hearts were examined with HE staining and Masson's trichrome staining. The protein expression was evaluated by Western blot, immunohistochemistry and immunofluorescence assays. The activities of sirtuin-1 (SIRT-1) and the content of NAD+ were detected with the corresponding test kits. Treatment with 6014 dose-dependently improved cardiac function, including LVEF, CO and SV and reversed the changes of cardiac structure in Ang II-infused mice: it significantly ameliorated Ang II-induced cardiac hypertrophy evidenced by attenuating the enlargement of cardiomyocytes, decreased HW/BW and LVW/BW, and decreased expression of hypertrophic markers ANF, BNP and ß-MHC; it also prevented Ang II-induced cardiac fibrosis, as implied by the decrease in excess accumulation of extracellular matrix (ECM) components collagen I, collagen III and FN. Further studies revealed that treatment with 6014 did not affect the expression levels of PARP-1, but dose-dependently inhibited the activity of PARP-1 and subsequently restored the activity of SIRT-1 in heart tissues due to the decreased consumption of NAD+ and attenuated Poly-ADP-ribosylation (PARylation) of SIRT-1. In conclusion, the novel PARP-1 inhibitor 6014 effectively protects mice against AngII-induced cardiac remodeling and improves cardiac function. Thus, 6014 might be a potential therapeutic agent for heart diseases..


Assuntos
Cardiomegalia/terapia , Cardiotônicos/uso terapêutico , Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores , Tioglicolatos/uso terapêutico , Remodelação Ventricular/efeitos dos fármacos , Xantinas/uso terapêutico , Angiotensina II/farmacologia , Animais , Cardiomegalia/induzido quimicamente , Cardiotônicos/síntese química , Fibrose/induzido quimicamente , Fibrose/terapia , Masculino , Camundongos Endogâmicos C57BL , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Sirtuína 1/metabolismo , Tioglicolatos/síntese química , Xantinas/síntese química
6.
Transl Res ; 166(5): 459-473.e3, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26118953

RESUMO

Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) is a crucial coregulator interacting with multiple transcriptional factors in the regulation of cardiac hypertrophy. The present study revealed that PGC-1α protected cardiomyocytes from hypertrophy by suppressing calcineurin-nuclear factor of activated T cells c4 (NFATc4) signaling pathway. Overexpression of PGC-1α by adenovirus infection prevented the increased protein and messenger RNA expression of NFATc4 in phenylephrine (PE)-treated hypertrophic cardiomyocytes, whereas knockdown of PGC-1α by RNA silencing augmented the expression of NFATc4. An interaction between PGC-1α and NFATc4 was observed in both the cytoplasm and nucleus of neonatal rat cardiomyocytes. Adenovirus PGC-1α prevented the nuclear import of NFATc4 and increased its phosphorylation level of NFATc4, probably through repressing the expression and activity of calcineurin and interfering with the interaction between calcineurin and NFATc4. On the contrary, PGC-1α silencing aggravated PE-induced calcineurin activation, NFATc4 dephosphorylation, and nuclear translocation. Moreover, the binding activity and transcription activity of NFATc4 to DNA promoter of brain natriuretic peptide were abrogated by PGC-1α overexpression but were enhanced by PGC-1α knockdown. The effect of PGC-1α on suppressing the calcinuerin-NFATc4 signaling pathway might at least partially contribute to the protective effect of PGC-1α on cardiomyocyte hypertrophy. These findings provide novel insights into the role of PGC-1α in regulation of cardiac hypertrophy.


Assuntos
Cardiomegalia/prevenção & controle , Miócitos Cardíacos/metabolismo , Fatores de Transcrição NFATC/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Transdução de Sinais , Fatores de Transcrição/fisiologia , Animais , Cardiomegalia/metabolismo , Masculino , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo , Ratos , Ratos Sprague-Dawley
7.
Arch Biochem Biophys ; 565: 76-88, 2015 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-25436917

RESUMO

Adipose triglyceride lipase (ATGL), the rate-limiting enzyme of triglyceride (TG) hydrolysis, plays an important role in TG metabolism. ATGL knockout mice suffer from TG accumulation and die from heart failure. However, the mechanisms underlying cardiac hypertrophy caused by ATGL dysfunction remain unknown. In this study, we found that ATGL expression declined in pressure overload-induced cardiac hypertrophy in vivo and phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. ATGL knockdown led to cardiomyocyte hypertrophy, while ATGL overexpression prevented PE-induced hypertrophy. In addition, ATGL downregulation increased but ATGL overexpression reduced the contents of ceramide, which has been proved to be closely associated with cardiac hypertrophy. Moreover, the accumulation of ceramide was due to elevation of free fatty acids in ATGL-knockdown cardiomyocytes, which could be explained by the reduced activity of peroxisome proliferator-activated receptor (PPAR) α leading to imbalance of fatty acid uptake and oxidation. These observations suggest that downregulation of ATGL causes the decreased PPARα activity which results in the imbalance of FA uptake and oxidation, elevating intracellular FFA contents to promote the accumulation of ceramides, and finally inducing cardiac hypertrophy. Upregulation of ATGL could be a strategy for ameliorating lipotoxic damage in cardiac hypertrophy.


Assuntos
Cardiomegalia/enzimologia , Ceramidas/metabolismo , Regulação Enzimológica da Expressão Gênica , Lipase/biossíntese , Miócitos Cardíacos/enzimologia , Animais , Cardiomegalia/genética , Cardiomegalia/patologia , Ceramidas/genética , Técnicas de Silenciamento de Genes , Lipase/genética , Masculino , Camundongos , Miócitos Cardíacos/patologia , Oxirredução , PPAR alfa/genética , PPAR alfa/metabolismo , Ratos , Ratos Sprague-Dawley
8.
Curr Vasc Pharmacol ; 13(4): 492-503, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25360840

RESUMO

OBJECTIVE: To reveal the cutoff point and influencing factors in the dynamic change in phenotypic group in patients with stable angina pectoris (SAP) after Xinxuekang capsule treatment. METHODS: Five hundred and seventy-six SAP patients were randomly assigned to receive Xinxuekang (XXK) capsules or Compound Danshen (CDS) tablets for 8 weeks. Global similarity degree analysis and nonlinear mixed effects modeling (NONMEM) were employed to reveal the cutoff points and influencing factors in dynamic changes in the SAP phenotypic group. The phenotypic group was defined as the six phenotypes in SAP, including angina, choking sensation in the chest, palpitations, dark purple lips, ecchymosis on the tongue, and fine-choppy pulse, which were quantitatively evaluated on Days 0, 14, 28, 42, and 56. RESULTS: Variation in the six individual phenotypes and distribution of the SAP phenotypic profile were similar between the two experimental groups, but cutoff points for changes in the SAP phenotypic group were 7.28 and 10.73 weeks in XXK and CDS groups, respectively. Degree of severity of SAP as well as study site significantly affected the tendency for change in the SAP Xueyu Zheng in both XXK and CDS treatment groups. Different Chinese patent drugs affected the tendency for change in phenotypic group in patients with SAP. XXK was superior to CDS in controlling a clinical phenotypic group. CONCLUSION: Based on global similarity degree analysis and NONMEM, the cutoff point and influencing factors in phenomic variation of SAP may be determined, to improve the development and modification of treatment regimens.


Assuntos
Angina Estável/diagnóstico , Angina Estável/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêutico , Medicina Tradicional Chinesa/métodos , Adulto , Idoso , Cápsulas , Interpretação Estatística de Dados , Método Duplo-Cego , Medicamentos de Ervas Chinesas/administração & dosagem , Humanos , Pessoa de Meia-Idade , Resultado do Tratamento
9.
Mol Cell Endocrinol ; 392(1-2): 14-22, 2014 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-24859603

RESUMO

Poly(ADP-ribose) polymerase-1 (PARP-1) enzyme, as a sensor of DNA damage, could convert nicotinamide adenine dinucleotide (NAD) into long poly(ADP-ribose) chains and regulate many cellular processes, including DNA repair, gene transcription, cell survival and chromatin remodeling. However, excessive activation of PARP-1 depletes its substrate NAD and leads to cell death. Mounting evidences have shown that PARP-1 overactivation plays a pivotal role in the pathogenesis of cardiac hypertrophy and heart failure. In present study, a novel PARP-1 inhibitor AG-690/11026014 (6014) was identified based on virtual screening and validated by bioassay. Our results further showed that 6014 prevented the cardiomyocytes from AngII-induced hypertrophy, accompanying attenuation of the mRNA and protein expressions of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP), and reduce in the cell surface area. Additionally, 6014 reversed the depletion ofcellular NAD and SIRT6 deacetylase activity induced by AngII in cardiomyocytes. These observations suggest that anti-hypertrophic effect of 6014 might be partially attributed to the rescue of NAD depletion and subsequent restoring of SIRT6 activity by inhibition of PARP-1. Moreover, 6014 attenuated the generation of oxidative stress via suppression of NADPH oxidase 2 and 4, which might probably contribute to the inhibition of PARP-1.


Assuntos
Cardiomegalia/enzimologia , Cardiomegalia/prevenção & controle , Cardiotônicos/uso terapêutico , Citoproteção/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Miócitos Cardíacos/patologia , Inibidores de Poli(ADP-Ribose) Polimerases , Tioglicolatos/farmacologia , Xantinas/farmacologia , Angiotensina II , Animais , Cardiotônicos/farmacologia , Avaliação Pré-Clínica de Medicamentos , Ativação Enzimática/efeitos dos fármacos , Inibidores Enzimáticos/análise , Inibidores Enzimáticos/química , Humanos , Concentração Inibidora 50 , Glicoproteínas de Membrana/metabolismo , Simulação de Acoplamento Molecular , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/enzimologia , NAD/metabolismo , NADPH Oxidase 2 , NADPH Oxidase 4 , NADPH Oxidases/metabolismo , Poli(ADP-Ribose) Polimerases/metabolismo , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio/metabolismo , Proteínas Recombinantes/metabolismo , Sirtuínas/metabolismo , Tioglicolatos/análise , Tioglicolatos/química , Regulação para Cima/efeitos dos fármacos , Xantinas/análise , Xantinas/química
10.
World J Gastroenterol ; 16(8): 1025-30, 2010 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-20180245

RESUMO

AIM: To investigate differential points of solid-pseudopapillary neoplasm (SPN) of the pancreas and pancreatic endocrine tumor (PET). METHODS: Ten cases of SPN and fourteen cases of PET were studied in this retrospective study. Clinical and pathologic features, immunostaining reactions and beta-catenin gene mutations were analyzed. RESULTS: The mean age of SPN patients was 25.6 years and these patients had no specific symptoms. The mean diameter of the tumors was 11.0 cm, 9/10 cases were cystic or a mixture of solid and cystic structures, and there was hemorrhage and necrosis on the cut surface in 8/10 (80%) cases. Characteristic pseudopapillary structure and discohesive appearance of the neoplastic cells were observed in all 10 (100%) cases. The results of immunostaining showed that nuclear expression of beta-catenin and loss of E-cadherin in all the cases, was only seen in SPN. Molecular studies discovered that 9/10 (90%) cases harbored a point mutation of exon 3 in beta-catenin gene. On the other hand, the mean age of PET patients was 43.1 years. Eight of 14 cases presented with symptoms caused by hypoglycemia, and the other 6 cases presented with symptoms similar to those of SPN. The mean size of the tumors was 2.9 cm, most of the tumors were solid, only 3/14 (21%) were a mixture of solid and cystic structures, and macroscopic hemorrhage and necrosis were much less common (3/14, 21%). Histologically, tumor cells were arranged in trabecular, acinar or solid patterns and demonstrated no pseudopapillary structure and discohesive appearance in all 14 (100%) cases. The results of immunostaining and mutation detection were completely different with SPN that membrane and cytoplastic expression of beta-catenin without loss of E-cadherin, as well as no mutation in beta-catenin gene in all the cases. CONCLUSION: Both macroscopic and microscopic features of SPN are quite characteristic. It is not difficult to distinguish it from PET. If necessary, immunostaining of beta-catenin and E-cadherin is quite helpful to make the differential diagnosis.


Assuntos
Neoplasias das Glândulas Endócrinas/diagnóstico , Neoplasias das Glândulas Endócrinas/patologia , Neoplasias Pancreáticas/diagnóstico , Neoplasias Pancreáticas/patologia , Adolescente , Adulto , Sequência de Bases , Caderinas/genética , Caderinas/metabolismo , Análise Mutacional de DNA , Neoplasias das Glândulas Endócrinas/genética , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Dados de Sequência Molecular , Mutação , Pâncreas/anatomia & histologia , Pâncreas/metabolismo , Pâncreas/patologia , Neoplasias Pancreáticas/genética , Estudos Retrospectivos , Adulto Jovem , beta Catenina/genética , beta Catenina/metabolismo
11.
Zhongguo Zhong Yao Za Zhi ; 32(10): 909-12, 2007 May.
Artigo em Chinês | MEDLINE | ID: mdl-17655142

RESUMO

OBJECTIVE: To explore the effect of compound decoction on notoginsenosides in Panax notoginseng. METHOD: Notoginsenoside R1, Rg1, Re, Rb1 and pH were used as the parameters to investigate the changes on the content of notoginsenosides in different compound extractions by heating for two hours and their correlation with pH. RESULT: When the pH values of solution of P. notoginseng with Fructus ligustri, P. notoginseng with Eupolyphaga seu steleophaga, P. notoginseng with Pheretima asiatica, and Zhitangjiang Fang (free of Hirudo) were rept higher than 5.7, the reserved rate (RR) of notoginsenside were higher than 90%; When the pH values of decoetion of P. notoginseng with Salvia miltiorrhiza, P. notoginseng with Paeonia lactiflora, P. notoginseng with Platycodon grandiflorum, P. notoginseng with Arctium lappa were kept 4.5-5.5, their RR of notoginsenside were 60% - 85%; When the pH values of the decotction of P. notoginseng with Hirudo nipponica was decreased to 3.4, its RR of of notoginsenside was 38.4%; When the pH values of Zhitangjiang Fang extraction was regulated by 0.1% NaOH solution to pH 6. 3, and the RR of notoginsenside increased to 97%. CONCLUSION: The pH of other Chinese herbal medicines extraction with P. notoginseng compound is a critical effect on the stability and yields of notoginsensides.


Assuntos
Medicamentos de Ervas Chinesas/química , Ginsenosídeos/análise , Panax/química , Animais , Arctium/química , Baratas/química , Combinação de Medicamentos , Medicamentos de Ervas Chinesas/isolamento & purificação , Hirudo medicinalis/química , Temperatura Alta , Concentração de Íons de Hidrogênio , Ligustrum/química , Materia Medica/química , Materia Medica/isolamento & purificação , Oligoquetos/química , Paeonia/química , Platycodon/química , Salvia miltiorrhiza/química
12.
Zhongguo Zhong Yao Za Zhi ; 32(22): 2364-7, 2007 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-18257259

RESUMO

OBJECTIVE: To study the different manufacturers Vitmin C (Vc) Yinqiao tablets, and the quality of the analysis of the problem, to provide a theoretical basis for the correct evaluation of the quality of medicines and improving the standard drugs. METHOD: 11 manufacturers of 18 batches of samples for determination of the weight of the core tablets, powder samples were observed with microscope, determination of Vc, and the establishment of the Vc Yinqiao tablets HPLC method for determination of chlorogenic acid and arctigenin, chlorogenic acid and arctigenin in the samples were measured and compared. RESULT: There is a big difference of microscope and various measured results in different manufacturers products. CONCLUSION: Because different manufacturers to produce the same, there are big differences in the quality of the products.


Assuntos
Ácido Ascórbico/química , Ácido Clorogênico/análise , Medicamentos de Ervas Chinesas/química , Furanos/análise , Lignanas/análise , Arctium/química , Cromatografia Líquida de Alta Pressão , Combinação de Medicamentos , Medicamentos de Ervas Chinesas/isolamento & purificação , Medicamentos de Ervas Chinesas/normas , Lonicera/química , Plantas Medicinais/química , Controle de Qualidade , Comprimidos
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