Turmeric has long been used as a spice and food colouring agent in Asia. In the present investigation, the antimutagenic potential of curcumin was evaluated in Allium cepa root meristem cells. So far there is no report on the biological properties of curcumin in plant test systems. The root tip cells were treated with sodium azide at 200 and 300 microg/ml for 3 h and curcumin was given at 5, 10 and 20 microg/ml for 16 h, prior to sodium azide treatment. The tips were squashed after colchicine treatment and the cells were analyzed for chromosome aberration and mitotic index. Curcumin induces chromosomal aberration in Allium cepa root tip cells in an insignificant manner, when compared with untreated control. Sodium azide alone induces chromosomal aberrations significantly with increasing concentrations. The total number of aberrations was significantly reduced in root tip cells pretreated with curcumin. The study reveals that curcumin has antimutagenic potential against sodium azide induced chromosomal aberrations in Allium cepa root meristem cells. In addition, it showed mild cytotoxicity by reducing the percentage of mitotic index in all curcumin treated groups, but the mechanism of action remains unknown. The antimutagenic potential of curcumin is effective at 5 microg/ml in Allium cepa root meristem cells.
Antimutagenic Agents ; pharmacology ; Chromosome Aberrations ; drug effects ; Curcumin ; pharmacology ; Meristem ; drug effects ; genetics ; Mutagens ; toxicity ; Onions ; drug effects ; genetics ; Sodium Azide ; toxicity

Amyloid beta-Peptides ; analysis ; Animals ; Frontal Lobe ; drug effects ; physiology ; Hippocampus ; drug effects ; physiology ; Learning ; drug effects ; Memory ; drug effects ; Rats ; Rats, Wistar ; Sodium Azide ; pharmacology ; Space Perception

Biocompatible silica-overcoated magnetic nanoparticles containing an organic fluorescence dye, rhodamine B isothiocyanate (RITC), within a silica shell [50 nm size, MNP@SiO2(RITC)s] were synthesized. For future application of the MNP@SiO2(RITC)s into diverse areas of research such as drug or gene delivery, bioimaging, and biosensors, detailed information of the cellular uptake process of the nanoparticles is essential. Thus, this study was performed to elucidate the precise mechanism by which the lung cancer cells uptake the magnetic nanoparticles. Lung cells were chosen for this study because inhalation is the most likely route of exposure and lung cancer cells were also found to uptake magnetic nanoparticles rapidly in preliminary experiments. The lung cells were pretreated with different metabolic inhibitors. Our results revealed that low temperature disturbed the uptake of magnetic nanoparticles into the cells. Metabolic inhibitors also prevented the delivery of the materials into cells. Use of TEM clearly demonstrated that uptake of the nanoparticles was mediated through endosomes. Taken together, our results demonstrate that magnetic nanoparticles can be internalized into the cells through an energy-dependent endosomal-lysosomal mechanism.
Biocompatible Materials/*pharmacokinetics ; Cell Line, Tumor ; Drug Delivery Systems/methods ; Endocytosis/*physiology ; Endosomes/physiology ; Humans ; Lung Neoplasms/drug therapy/*metabolism ; Macrolides/pharmacology ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Nanoparticles/*administration & dosage ; Sodium Azide/pharmacology ; Sucrose/pharmacology ; Temperature

OBJECTIVETo investigate the effects of Aloe vera extract (AV) on mitochondria in rat pheochromocytoma (PC12) cells and rat brain and to study the mechanism of its neuroprotection.

METHODAfter treatment, the morphology of PC12 cells was observed under microscope, the activity of mitochondria in PC12 cells was measured by MTT method, and the mitochondrial membrane potential (MMP) in PC12 cells was detected by JC-1 method. The mitochondrial function in rat brain was detected by resazurin method. The production of malondialdehyd (MDA) in rat brain mitochondria was tested by thiobarbaturic acid (TBA) assay.

RESULTAV could improve mitochondrial damage induced by azide sodium (NaN3) in PC12 cells. The viability of PC12 cells treated with NaN364 mmol x L(-1) for 4 h decreased by 47.8%, and AV at 1 and 10 mg x L(-1) could respectively increase the viability of NaN3-treated cells by 16.7% (P < 0.05) and 22.3% (P < 0.01). MMP in PC12 cells in AV 1 and 10 mg x L(-1) group was significantly higher than that of NaN3-treated group (P < 0.05). AV also protected the structure and function of mitochondria in rat brain. AV at 10 mg x L(-1) had protective effect on mitochondria function impair induced by NaN3 (P < 0.01). AV 1 and 10 mg x L(-1) markedly inhibited the lipid peroxidation of brain mitochondria induced by Fe2+ -cysteine (P < 0.05, P < 0.01).

CONCLUSIONAV has protective effects on mitochondria of neuronal cells and rat brain.

Aloe ; chemistry ; Animals ; Brain ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Malondialdehyde ; metabolism ; Mitochondria ; drug effects ; metabolism ; Neurons ; drug effects ; metabolism ; PC12 Cells ; Plant Extracts ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Sodium Azide ; pharmacology

This study is to investigate the protective effect of astaxanthin against injured hepatocyte L-02 cells induced by sodium azide (NaN3) and reveal the possible mechanisms. Hepatocyte L-02 cells were exposed to 100 mmol.L-1 NaN3 with various concentrations of astaxanthin pre-incubated, then the cell viability was measured by MTT method; The level of reactive oxygen species (ROS) was determined by DCFH-DA method; The changes of mitochondrial membrane potential (MMP) and apoptosis ratio were detected by JC-1 method and Annexin V-FITC/PI double stain method, respectively. Results showed that after cells were exposed to 100 mmol.L-1 NaN3 for 3 hours, the cell viability significantly decreased; ROS level and the percentage of late phase apoptosis increased obviously; MMP was also declined. When cells were pretreated with astaxanthin, the cell damage and late phase apoptosis ratio reduced and MMP was maintained. However, the level of ROS showed insignificant decrease (P>0.05). The beneficial concentration of astaxanthin in improving cell viability and MMP was not in a dose dependent manner and the most effective of which was 0.10 nmol.L-1 (P<0.01). In order to reveal its possible non-antioxidant mechanism, mitochondrial membrane was imitated and H+ transferring function of astaxanthin was also detected by bilayer lipid membrane (BLM) method. Results showed that 2.0% astaxanthin could transfer H+ efficiently. These suggested the mechanisms of astaxanthin in protection of hepatocyte L-02 cells not via its ROS quenching capability but via its H+ transferring function, which improved the mitochondrial function and had the sequence biology effects.
Antioxidants ; pharmacology ; Apoptosis ; drug effects ; Cell Line ; Cell Survival ; drug effects ; Hepatocytes ; cytology ; drug effects ; Humans ; Hydrogen-Ion Concentration ; Membrane Potential, Mitochondrial ; drug effects ; Protons ; Reactive Oxygen Species ; metabolism ; Sodium Azide ; toxicity ; Xanthophylls ; pharmacology

OBJECTIVETo observe the effect of synchronous perfusion of specific respiratory chain complex IV inhibitor sodium azide (NaN3) in brain on rat ventromedial prefrontal cortex (mPFC) and acetylcholine (ACh) and choline (Ch) contents in hippocampal extra-cellular fluid, and establish the AD rat model induced by mitochondrial acute injury.

METHODThe synchronous dual-probe dual-channel brain microdialysis sampling technology was applied to synchronously perfuse modified Ringer's solution containing NaN3 (50 micro mol L-1) and neostigmine (2 micro mol L-1) into mPFC and hippocampus of conscious, freely moving normal rats, and continuously collect dialysates from different encephalic areas. Dynamic contents of ACh and Ch were determined by high performance liquid chromatography-post-column immobilized enzyme reactor-electrochemical process.

RESULTACh and Ch contents in mPFC extracellular fluid of normal rats were higher than that in hippocampus. During the process of perfusion, NaN3 could significantly reduce ACh in mPFC/hippocampal extra-cellular fluid, but remarkably increase Ch, and constantly inhibit the recovery of ACh and Ch contents in mPFC/hippocampus.

CONCLUSIONThe synchronous perfusion of NaN3in rat mPFC and hippocampus can injure functions of the cholinergic nerve projection area, and cause the acute AD model with ACh and Ch metabolic disorders. This model can be used in pathogenetic and pharmacological studies.

Acetylcholine ; metabolism ; Animals ; Choline ; metabolism ; Extracellular Fluid ; drug effects ; metabolism ; Hippocampus ; cytology ; Male ; Neurotransmitter Agents ; metabolism ; Perfusion ; Prefrontal Cortex ; cytology ; Rats ; Rats, Sprague-Dawley ; Sodium Azide ; administration & dosage ; pharmacology ; Time Factors

The characteristics of uptake, transepithelial transport and efflux of Z- and E-ajoenes isolated from the bulbs of Allium sativum were studied. A human colon cell model Caco-2 cell monolayers in vitro cultured had been applied to study the characteristics of uptake, transepithelial transport and efflux of Z- and E-ajoenes. The quantitative determination of Z- and E-ajoenes was performed by high-performance liquid chromatography. Z- and E-Ajoenes can be detected only in the apical side and can be metabolized, but both compounds can not be transported from apical-to-basolateral and basolateral-to-apical directions in cultured Caco-2 cell monolayers. The metabolism of Z- and E-ajoenes in Caco-2 cell monolayers can be partially inhibited by vitamin C as an anti-oxidant, metyrapone as an inhibitor to subtype CYP3A of cytochrome P450 drug metabolism enzymes, and sodium azide as an inhibitor to ATP production. It is shown that neither Z-ajoene nor E-ajoene can pass through Caco-2 cell monolayers, and that they can be metabolized by the cells. The metabolism might be in correlation with cytochrome P450 drugs metabolism enzymes in Caco-2 cell monolayers.
Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Biological Transport ; drug effects ; Caco-2 Cells ; Cell Membrane ; drug effects ; metabolism ; Cytochrome P-450 CYP3A ; metabolism ; Cytochrome P-450 CYP3A Inhibitors ; Disulfides ; chemistry ; isolation & purification ; pharmacokinetics ; Enzyme Inhibitors ; pharmacology ; Garlic ; chemistry ; Humans ; Metyrapone ; pharmacology ; Plants, Medicinal ; chemistry ; Sodium Azide ; pharmacology ; Stereoisomerism

OBJECTIVETo investigate the protection mechanism of prepared Polygonum multiflorum (PPMT) in rat brain with sodium azide (NaN3) perfusion.

METHODRats were divided into six groups: control, model, PPMT, Duxil and PPMT + Duxil groups. The intracerebral microdialysis and high performance liquid chromatography-post column Immobilized enzyme reactor-electrochemical detection were used to continuously measure extracellular acetylcholine (ACh) and choline (Ch) levels in striatum of freely moving awake rats.

RESULTThe extracellular Ach, Ch levels of striatum stayed stable in the control group during the whole observing period, but the ACh levels in the model group were lower significant than that in the control group. The Ach levels of three drug groups were respectively higher significant than that of model group at some time points. While the extracellular Ch level in striatum of the model group increased singnificantly compared with the control group. The Ch levels of the three drug groups were lower significant than that of the model group respectively at certain time points. The effects of PPMT were similar with that of Duxil.

CONCLUSIONThe prepared P. multiflorum can improve the impaired cholinergic nerve function to exert the effects of brain protection by elevating extracellular Ach level and improving uptake of extracellular Ch. It may provide the experimental evidence to support the idea that P. multiflorum could be brain protective drug to treat retrogressive disease such as dementia.

Acetylcholine ; metabolism ; Animals ; Choline ; metabolism ; Corpus Striatum ; metabolism ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Male ; Mitochondria ; drug effects ; metabolism ; Mitochondrial Diseases ; chemically induced ; metabolism ; Neuroprotective Agents ; isolation & purification ; pharmacology ; Perfusion ; adverse effects ; Plants, Medicinal ; chemistry ; Polygonum ; chemistry ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sodium Azide

AIMTo study the protective effect of salidroside on mitochondria injury induced by sodium azide.

METHODSHuman neuroblastoma SH-SY5Y cells were exposed to sodium azide with different concentration of salidroside, then cell viability was measured by thiazolyl blue (MTT) method and mitochondrial membrane potential (MMP) was detected by JC-1 method. Protective effect of salidroside against disfunction of mitochondria induced by sodium azide was detected by resazurin method.

RESULTSAfter exposing to 64 mmol x L(-1) sodium azide for 4 hours, cell viability and MMP of SH-SY5Y cells significantly decreased. When pretreated with salidroside, the cell damage was greatly reduced and the mitochondrial membrane potential was maintained. Furthermore, salidroside can protect function of rat brain mitochondria against damage induced by sodium azide.

CONCLUSIONSalidroside was demonstrated to play an important role in improving the function of mitochondria.

Animals ; Brain Neoplasms ; pathology ; physiopathology ; Cell Line, Tumor ; Cell Survival ; Glucosides ; isolation & purification ; pharmacology ; Humans ; Male ; Membrane Potentials ; drug effects ; Mitochondria ; drug effects ; metabolism ; Neuroblastoma ; pathology ; physiopathology ; Oxidation-Reduction ; drug effects ; Phenols ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Rhodiola ; chemistry ; Sodium Azide

OBJECTIVETo investigate the effects of Tianzhi Keli (TZ) on acetylcholine (ACh) and catecholamine levels in striatum of rats with neuromitochondrial impairment, and try to find out the neuroprotective mechanism of TZ.

METHODThe microdialysis and high performance liquid chromatography (HPLC)-post column Immobilized enzyme reactor (IMER)-electrochemical detection (ED) were used to establish a model of mitochondrial energy metabolism impairment which induced by perfusion with sodium azide (NaN3), and measure continuously the effects of TZ on extracellular ACh, choline (Ch) and catecholamine of model rats.

RESULTAfter perfusion with NaN3, ACh, noradrenalin (NE), adrenaline (E), dopamine (DA), 3,4-Dihydroxyphenyl-aletic (DOPAC), and homovanillic acid (HVA) levels were decreased obviously (P < 0.05-0.01), while Ch level was increased distinctly (P < 0.01). Transmitters levels were recovered individually after stop the perfusion with NaN3. TZ can postpone the decrease of ACh and advance the recover of Ch. The effect of TZ coupled with duxil on increasing ACh level is more obviously than effect of TZ or duxil. TZ is also showing a tendency to postpone the decrease of catecholamine and advance its recovery. TZ coupled with duxil can advance the recovery of DOPAC and adjust the metabolic abnormity positively.

CONCLUSIONTZ has effect on protecting impairment of choline neurosystem, which induced by damage of mitochondrion and abnormity of energy metabolism; coupled with duxil have synergistic action. TZ also has tendency to protect the impairment of epinephrine and dopamine neurosystem.

3,4-Dihydroxyphenylacetic Acid ; metabolism ; Acetylcholine ; metabolism ; Animals ; Catecholamines ; metabolism ; Corpus Striatum ; metabolism ; Dopamine ; metabolism ; Drug Combinations ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Extracellular Space ; metabolism ; Gastrodia ; chemistry ; Male ; Microdialysis ; Mitochondrial Diseases ; chemically induced ; metabolism ; Norepinephrine ; metabolism ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Sodium Azide ; Uncaria ; chemistry