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1.
Acta Pharmaceutica Sinica ; (12): 166-169, 2024.
Artículo en Chino | WPRIM | ID: wpr-1005434

RESUMEN

A novel pair of Z/E isomeric compounds with unprecedented carbon skeleton were isolated from an aqueous extract of Aspongopus chinensis Dallas by macroporous resin, silica gel, and semi-preparative high performance liquid chromatography (HPLC). Their structures were identified by nuclear magnetic resonance (NMR), Infrared spectroscopy (IR), Mass spectroscopy (MS) and other spectroscopic methods as (Z)-3-(but-1″-en-1″-yl)-1-(2ʹ-hydroxyethyl)-4-propylpyridin-1-ium, namely aspongopyridine A, and (E)-3-(but-1″-en-1″-yl)-1-(2ʹ-hydroxyethyl)-4-propylpyridin-1-ium, namely aspongopyridine B, respectively. Besides, the anti-inflammatory, anti-tumor, acetylcholinesterase inhibition and butyrylcholinesterase inhibition activities of the compounds 1 and 2 were evaluated. The results showed that compounds 1 and 2 have no anti-inflammatory, anti-tumor, and butyrylcholinesterase inhibition activities instead of weak acetylcholinesterase inhibition activity.

2.
Journal of Pharmaceutical Analysis ; (6): 683-688, 2023.
Artículo en Chino | WPRIM | ID: wpr-991174

RESUMEN

During the analysis of benziamidazole-class irreversible proton pump inhibitors,an unusual mass spectral response with the mass-to-charge ratio at[M+10]+intrigued us,as it couldn't be assigned to any literature known relevant structure,intermediate or adduct ion.Moreover,this mysterious mass pattern of[M+10]+has been gradually observed by series of marketed proton pump inhibitors,viz.omeprazole,pantoprazole,lansoprazole and rabeprazole.All the previous attempts to isolate the corresponding component were unsuccessful.The investigation of present work addresses this kind of signal to a pyridinium thiocyanate mass spectral intermediate(10),which is the common fragment ion of series of labile aggregates.The origin of such aggregates can be traced to the reactive intermediates formed by acid-promoted degradation.These reactive intermediates tend to react with each other and give raise series of complicated aggregates systematically in a water/acetonitrile solution by electrospray ioniza-tion.The structure of the corresponding pyridinium thiocyanate species of omeprazole(10a)has been eventually characterized with the help of synthetic specimen(10a').Our structural proposal as well as its origin was supported by in situ nuclear magnetic resonance,chemical derivatization and colorimetric experiments.

3.
Artículo en Inglés | IMSEAR | ID: sea-159975

RESUMEN

Background: Cetyl pyridinium chloride (CPC) liquefied sputum was shown to reduce AFB smear positivity presumably damaging cell wall of M. tuberculosis. Settings: National Institute for Research in Tuberculosis, Chennai, (Tamil Nadu). Objective: To assess the cell wall damage of mycobacteria in CPC liquefied sputum, by Transmission Electron Microscopy (TEM) and mycobacteriophage adsorption studies. Methods: Pooled sputum sample from smear positive pulmonary TB patients was homogenized and liquefied with CPC. It was examined in TEM daily for four days, to assess cell wall damage of M. tuberculosis, and photomicrographs were taken. M. smegmatis mc2155, treated with CPC, was infected with mycobacteriophage (phAE129) to study phage adsorption on cell wall and plaque formation. CPC untreated sputum and M. smegmatis formed controls. Results: Photomicrographs showed that cell wall of M. tuberculosis was intact in controls and damaged in CPC preserved sputum for 96 hours. Plaque formation was seen and absent respectively in CPC untreated and treated M. smegmatis cells. Conclusion: Exposure to CPC damaged the cell wall of M. tuberculosis within 96 hours. Mycobacteriophage failed to form plaques after M. smegmatis mc2155 was treated with CPC implying inhibition of phage adsorption on damaged cell wall and thus providing a clue for poor staining and smear positivity in microscopy.


Asunto(s)
Pared Celular/química , Pared Celular/fisiología , Cetilpiridinio/fisiología , Microscopía Electrónica de Transmisión/métodos , Micobacteriófagos/citología , Micobacteriófagos/fisiología , Mycobacterium tuberculosis/citología , Mycobacterium tuberculosis/fisiología
4.
Yonsei Medical Journal ; : 435-440, 2002.
Artículo en Inglés | WPRIM | ID: wpr-198781

RESUMEN

Secondary osteoporosis is a feature of rheumatoid arthritis (RA). In recent years, several attempts have been made to develop specific markers for monitoring connective tissue metabolism in arthritic diseases. Our purpose, in this study was to assess pyridinium crosslinks (PYD and DPYD) excretion in relation to the activity of RA (changes related to sulphasalazine treatment). Fourty premenopausal female patients with active RA (mean age; 36.0 7.2 years), 20 postmenopausal women with active RA (mean age; 60.0 6.8 years), 23 postmenopausal women with OA (mean age; 56.1 6.6 years) and 17 premenopausal healthy subjects (mean age; 28.3 4.28 years) were enrolled in our study. All of the 40 premenopausal female patients with active RA were given sulphasalazine. The mean follow up period for these patients was 10.3 1.1 months. In all of these patients, urine samples were collected both in the active and in the inactive periods. Urine PYD and DPYD levels were measured by ELISA. Urine PYD levels were significantly higher in the active period (14.01 3.16 nmol/mmol cr) than in the inactive (8.25 4.23 nmol/mmol cr) period in patients with premenopausal RA (p 0.05). Urine PYD levels were significantly high in postmenopausal active RA patients (19.06 3.26 nmol/mmol cr) compared to premenopausal active and ind inactive, postmenopausal inactive RA patients, osteoarthritis and healthy controls. Urine DPYD excretion was similar in patients with premenopausal RA in the active (7.46 2.13 nmol/mmol cr) and inactive periods (5.08 0.87 nmol/mmol cr) (p 0.05). In active premenopausal RA patients, a correlation was found between PYD excretion and RAI, ESR, CRP and functional capacity (r=0.5729 p 0.01, r=0.5953 p 0.01, r=0.6125 p 0.01 and r=0.6232, p 0.01 respectively). But in the inactive period, no such correlation was was evident. In disease activity parameters did not correlate with DPYD excretion in either the active or the inactive period. As a result, urine PYD excretion was significantly high in patients with active RA. During sulphasalazine treatment, urine PYD levels decreased. This is attributed to improvement in bone destruction.


Asunto(s)
Adulto , Anciano , Femenino , Humanos , Corticoesteroides/efectos adversos , Aminoácidos/orina , Artritis Reumatoide/orina , Colágeno/orina , Persona de Mediana Edad , Osteoporosis/orina , Sulfasalazina/farmacología
5.
Chinese Traditional and Herbal Drugs ; (24)1994.
Artículo en Chino | WPRIM | ID: wpr-681240

RESUMEN

Object To establish a rat cerebellar granular neuron (CGN) apoptosis model by 1 methy 4 phenyl pyridinium cation (MPP +) Methods Rat CGN were treated with MPP + and the resulting cell morphology examined by methyl green pyronine staining, agarose gel electrophorsis of DNA and flow cytometry Results MPP + at the concentration of 50 ? mol/L can induce CGNs apoptosis of the established model Conclusion The CGNs apoptosis model induced by MPP + can be used for the study on regulatory mechanism of cell apoptosis and the screening of antiparkinsonian drugs

6.
Journal of Clinical Neurology ; (6)1993.
Artículo en Chino | WPRIM | ID: wpr-586790

RESUMEN

Objective To observe the effects of MPP+ on the expression of inhibin, activin and its receptor ⅡA and cell ability in PC12 cells of rats.Methods The changes of expression of activin?A, activin?B, inhibin? and receptorⅡA mRNAs were assayed by RT-PCR, the change of cell viability was detect by tyrpan blue exclusion method in cultured PC12 cells at 3 h,6 h,12 h,24 h after MPP+ was added and compared with control groups.Results The expression of activin?A, activin?B and activin receptorⅡA mRNAs in PC12 cells were down-regulated significantly after MPP+ administrated at every time point while the expression of inhibin? mRNA remained unchanged. The cell viability decreased at the points of 12 h and 24 h after MPP+ administrated.Conclusion MPP+ may cause the injury of PC12 cells by downregulating the expression of activin and its receptor.

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