Determination of gemfibrozil by HPLC in pharmacokinetic studies

Kadenatsi, I. B.; Levchuk, S. N.; Agapitova, I. V.; Глезер, М. Г.; Dombrovskii, V. S.; Mukumov, M R; Firsov, Alexander A.

doi:10.1007/bf02219538

Cited by 5 publications

(4 citation statements)

References 4 publications

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“…The concentration of gemfibrozil in mouse brain was measured as described earlier by Kadenatsi et al (1995) with some modifications. In brief, 100 mg of brain tissue of each mice was homogenized in 1 ml of chloroform/ methanol/perchloric acid (2:1:0.05), and the homogenate was centrifuged at 10,000g for 10 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Gemfibrozil Ameliorates Relapsing-Remitting Experimental Autoimmune Encephalomyelitis Independent of Peroxisome Proliferator-Activated Receptor-α

Dasgupta

Roy²,

Jana³

et al. 2007

Mol Pharmacol

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The present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of peroxisome proliferatoractivated receptor-␣ (PPAR-␣), in inhibiting the disease process of adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of relapsing-remitting multiple sclerosis. Clinical symptoms of EAE, infiltration of mononuclear cells, and demyelination were significantly lower in SJL/J female mice receiving gemfibrozil through food chow than those without gemfibrozil. It is noteworthy that the drug was equally effective in treating EAE in PPAR-␣ wild-type as well as knockout mice. Gemfibrozil also inhibited the encephalitogenicity of MBP-primed T cells and switched the immune response from a Th1 to a Th2 profile independent of PPAR-␣. Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-␥ (IFN-␥) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4. Gemfibrozil treatment decreased the number of T-bet-positive T cells and increased the number of GATA3-positive T cells in spleen of donor mice. The histological and immunohistochemical analyses also demonstrate the inhibitory effect of gemfibrozil on the invasion of T-bet-positive T cells into the spinal cord of EAE mice. Furthermore, we demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due to its inhibitory effect on NO production. Although excess NO favored the expression of T-bet, scavenging of NO stimulated the expression of GATA-3. Taken together, our results suggest gemfibrozil, an approved drug for hyperlipidemia in humans, may find further therapeutic use in multiple sclerosis.Multiple sclerosis (MS) is one of the most common neurological diseases affecting young adults. Although the etiology of MS is not completely understood, studies of patients with MS suggest that the observed demyelination in the CNS is a result of a T-cell-mediated autoimmune response (Martin et al., 1992). Experimental allergic encephalomyelitis (EAE) serves as an animal model for MS (Tuohy et al., 1988;Benveniste, 1997;Du et al., 2001). Studies using the adoptively transferred EAE model strongly support the view that activated neuroantigen-specific T cells cross the blood-brain barrier, infiltrate the CNS parenchyma, and initiate an inflammatory response (Tuohy et al., 1988;Benveniste, 1997). The identification of wide range of proinflammatory cytokines, cell adhesion molecules, chemokines, proinflammatory enzymes such as inducible nitric-oxide synthase (iNOS) and cyclooxygenase in CNS lesions of patients with MS and animals with EAE (Martin et al., 1992;Benveniste, 1997) suggests that the inflammatory process initiated by activated T cells eventually becomes a broad-spectrum one. Therefore, analysis of molecular mechanisms for the regulation of this broad-spectrum inflammatory process in EAE should help decipher the mechanisms of the disease process in MS/EAE and further the p...

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Section: Methodsmentioning

confidence: 99%

Gemfibrozil Ameliorates Relapsing-Remitting Experimental Autoimmune Encephalomyelitis Independent of Peroxisome Proliferator-Activated Receptor-α

Dasgupta

Roy²,

Jana³

et al. 2007

Mol Pharmacol

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“…The mechanism of this action is not completely understood but may involve inhibition of peripheral lipolysis; reduced hepatic extraction of free fatty acids, which reduces hepatic triglyceride production; inhibition of synthesis and increased clearance of VLDL carrier, apolipoprotein B, which also reduces VLDL production and according to animal studies, reduced incorporation of longchain fatty acids into newly formed triglycerides, accelerated turnover and removal of cholesterol from the liver (stimulates incorporation of cholesterol precursors into precursors into liver sterols), and increased excretion of cholesterol in the feces [4][5][6][7][8][9] . Gemfibrozil is determined by high performance liquid chromatography (HPLC) [10][11][12][13] , liquid chromatography (LC) 14,15 , gas chromatography (GC) 16 19 , ion exchange 20 , hydrophobicity interaction 21 , and electrostatic interaction [22][23] . To our best knowledge, there are no reports for quantitative determination of gemfibrozil by using poly (gabapentin) film modified glassy carbon electrode.…”

Section: Introductionmentioning

confidence: 99%

Cyclic Voltammetric Studies of Gemfibrozil at Poly (Gabapentin) Film Modified Glassy Carbon Electrode

P¹,

Deepa²,

Naik³

et al. 2012

Int J Pharmceut Chem

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ABSTRACT:A polymerized film of gabapentin was prepared on the surface of a glassy carbon electrode (GCE) in phosphate buffer solution by electropolymerisation method using cyclic voltammetric technique. The poly (gabapentin) film modified glassy carbon electrode was calibrated with standard potassium ferrocyanide solution in 1 M KCl as a supporting electrolyte. This modified electrode used to study the electrochemical behavior of gemfibrozil, a lipid lowering drug in aqueous alcohol medium by cyclic voltammetric technique. It was found that the oxidation peak current of gemfibrozil at the modified GCE was greatly improved compared with that at the bare GCE. The effects of scan rate, pH, supporting electrolyte concentration, % of solvent and concentration of gemfibrozil were examined. With high sensitivity and selectivity, micro molar detection limit, high reproducibility together with ease of preparation and regeneration of the electrode surface make the electrode very stable for the determination of gemfibrozil in pharmaceutical and clinical preparations.

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“…Several reports on gemfibrozil determination have appeared in the literature. Gas chromatography [11] and high performance liquid chromatography (HPLC) with ultraviolet or fluorimetric detection [12][13][14][15][16][17][18][19] have been used for the determination of gemfibrozil and its metabolites in plasma and urine samples. A liquid chromatography-mass spectrometric method [20] has been reported for the determination of this drug in water and wastewater samples.…”

Section: Introductionmentioning

confidence: 99%

Development of a new analytical spectroscopic methodology based on the competitive aggregation in a dye–surfactant–drug system: Application to the determination of gemfibrozil

2008

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Abstract.A new analytical methodology based on the competitive aggregation in a dye-surfactant-drug system is developed for the determination of gemfibrozil. Eriochrome Blue Black R (EBBR) and Didodecyldimethylammonium bromide (DDABr) were the dye and surfactant used, respectively. In the proposed method, the anions of the dye bind to the cationic surfactant molecules to form dye-surfactant aggregates, which are monitored from changes in UV-Vis absorption features of the dye. In the ternary EBBR-DDABr-drug mixtures, the drug competes with the dye to interact with the surfactant, which results in a decrease in dye-surfactant aggregates formation. This, again, causes a change in absorption properties of the dye. The measurement parameter is the difference between the absorption of the dye in the presence and absence of the drug. In the appropriate experimental conditions the absorbance differences are directly proportional to the drug concentration. The influence of several experimental variables such as pH, concentrations of buffer, EBBR and DDABr on the measurement parameter were studied. Under the optimum conditions, the calibration graph was linear up to 6.0 µg ml −1 with the correlation coefficient of 0.998.The limit of detection and quantification were found to be 0.044 and 0.15 µg ml −1 , respectively. The method was validated and applied to the determination of gemfibrozil in pharmaceutical preparations.

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Determination of gemfibrozil by HPLC in pharmacokinetic studies

Cited by 5 publications

References 4 publications

Gemfibrozil Ameliorates Relapsing-Remitting Experimental Autoimmune Encephalomyelitis Independent of Peroxisome Proliferator-Activated Receptor-α

Gemfibrozil Ameliorates Relapsing-Remitting Experimental Autoimmune Encephalomyelitis Independent of Peroxisome Proliferator-Activated Receptor-α

Cyclic Voltammetric Studies of Gemfibrozil at Poly (Gabapentin) Film Modified Glassy Carbon Electrode

Development of a new analytical spectroscopic methodology based on the competitive aggregation in a dye–surfactant–drug system: Application to the determination of gemfibrozil

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