ABSTRACT
CONTEXT: Rhizophora mucronata Lam. (Rhizophoraceae), commonly known as Asiatic mangrove, has been used traditionally among Asian countries as folk medicine. OBJECTIVE: This study investigates the cholinesterase inhibitory potential and antioxidant activities of R. mucronata. MATERIALS AND METHOD: Rhizophora mucronata leaves were successively extracted using solvents of varying polarity and a dosage of 100-500 µg/ml were used for each assay. Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inhibitory activities were assessed according to the method of Ellman. In vitro antioxidant activity was assessed using free radical scavenging, reducing power, and metal-chelating activity (duration - 3 months). Total phenolic and flavonoid content were quantified spectrophotometrically. Compound characterization was done using column chromatography, NMR, FTIR, and LC-MS analysis. RESULTS: Methanolic leaf extract (500 µg/ml) exhibited the highest inhibitory activity against AChE (92.73 ± 0.54%) and BuChE (98.98 ± 0.17%), with an IC50 value of 59.31 ± 0.35 and 51.72 ± 0.33 µg/ml, respectively. Among the different solvent extracts, methanolic extract exhibited the highest antioxidant activity with an IC50 value of 47.39 ± 0.43, 401.45 ± 18.52, 80.23 ± 0.70, and 316.47 ± 3.56 µg/ml for DPPH, hydroxyl, nitric oxide radical, and hydrogen peroxide, respectively. Total polyphenolic and flavonoid contents in methanolic extract were observed to be 598.13 ± 1.85 µg of gallic acid equivalent and 48.85 ± 0.70 µg of rutin equivalent/mg of extract. Compound characterization illustrated (+)-catechin as the bioactive compound responsible for cholinesterase inhibitory and antioxidant activities. CONCLUSION: The presence of rich source of flavonoids, in particular catechin, might be responsible for its cholinesterase inhibitory and antioxidant activities.
Subject(s)
Cholinesterase Inhibitors/pharmacology , Free Radical Scavengers/pharmacology , Neuroprotective Agents/pharmacology , Plant Extracts/pharmacology , Rhizophoraceae/chemistry , Acetylcholinesterase/metabolism , Butyrylcholinesterase/metabolism , Cholinesterase Inhibitors/chemistry , Cholinesterase Inhibitors/isolation & purification , Chromatography, High Pressure Liquid , Dose-Response Relationship, Drug , Free Radical Scavengers/chemistry , Free Radical Scavengers/isolation & purification , Kinetics , Magnetic Resonance Spectroscopy , Neuroprotective Agents/chemistry , Neuroprotective Agents/isolation & purification , Phytotherapy , Plant Extracts/chemistry , Plant Extracts/isolation & purification , Plant Leaves , Plants, Medicinal , Solvents/chemistry , Spectrometry, Mass, Electrospray Ionization , Spectroscopy, Fourier Transform InfraredABSTRACT
Nowadays, dietary guidelines acknowledge the therapeutic role of omega-3 polyunsaturated fatty acids, as the most important class of fatty acids, against different human diseases. During the last two decades, the average level of consumption of omega-3 polyunsaturated fatty acids has increased from 0.1 to 0.2 g per day. Omega-3 polyunsaturated fatty acids are a group of long-chain polyunsaturated fatty acids which are identified in different foods such as fatty fish, shellfish, and vegetable oils. A growing body of epidemiological and experimental evidence supports the anticancer effects of omega-3 polyunsaturated fatty acids, which led to the identification of their molecular targets in several cancer models. The present review focuses on the basic evidence supporting the potential applications of omega-3 polyunsaturated fatty acids in cancer therapy.
Subject(s)
Anticarcinogenic Agents/therapeutic use , Antineoplastic Agents/therapeutic use , Fatty Acids, Omega-3/therapeutic use , Neoplasms/drug therapy , Anticarcinogenic Agents/pharmacology , Antineoplastic Agents/pharmacology , Cell Death/drug effects , Cell Proliferation/drug effects , Fatty Acids, Omega-3/pharmacology , Humans , Inflammation/metabolism , Molecular Targeted Therapy , Neoplasm Metastasis , Neoplasms/blood supply , Neoplasms/metabolism , Neoplasms/pathology , Neovascularization, Pathologic/drug therapy , Neovascularization, Pathologic/pathology , Signal Transduction/drug effects , Transcription Factors/antagonists & inhibitorsABSTRACT
Benzo(a)pyrene (B(a)P), which is commonly used as an indicator species for polycyclic aromatic hydrocarbon (PAH) contamination, has a large number of hazardous consequences on human health. In the presence of the enzyme cytochrome-P-450 1A1 (CYP1A1), it undergoes metabolic activation to form reactive intermediates that are capable of inducing mutagenic, cytotoxic, teratogenic and carcinogenic effects in various species and tissues. Research within the last few years has shown that flavonoids exhibit chemopreventive effect against these toxins. In the present study, the protective effect of silymarin (a flavonoid) against B(a)P-induced toxicity was monitored in Wistar rats by evaluating the levels of hepatic phase I (CYP1A1), phase II enzymes (glutathione-S-transferase, epoxide hydroxylases, uridinediphosphate glucuronosyltransferases, NAD(P)H: quinone oxidoreductase 1, sulfotransferases), cellular antioxidant enzyme heme oxygenase and total glutathione. The results reveal that silymarin possesses substantial protective effect against B(a)P-induced damages by inhibiting phase I detoxification enzyme CYP1A1 and modulating phase II conjugating enzymes, which were confirmed by histopathological analysis. Overall, the inhibition of CYP1A1 and the modulation of phase II enzymes may provide, in part, the molecular basis for the effect of silymarin against B(a)P.
Subject(s)
Benzo(a)pyrene/toxicity , Chemical and Drug Induced Liver Injury/enzymology , Chemical and Drug Induced Liver Injury/prevention & control , Protective Agents/pharmacology , Silymarin/pharmacology , Animals , Cytochrome P-450 CYP1A1/metabolism , Dose-Response Relationship, Drug , Enzyme Activation , Enzyme Repression , Female , Liver/pathology , Rats , Rats, WistarABSTRACT
Polyphenols are the most abundant components of our daily food, occupying the major portion of naturally occurring phytochemicals in plants. Currently, polyphenols have received a special attention from the scientific community against health risk because of their antioxidant capacity and the ability to scavenge the free radicals formed during the pathological process like cancer, cardiovascular diseases and neurodegenerative disorders. Alzheimer's disease, one of the common forms of dementia is an intricate, multifactorial mental illness which is characterized by age-dependent memory loss ultimately leading to a steady decline of cognitive function. Extracellular amyloid beta deposition and intracellular tau hyperphosphorylation are the two main alterations occurring in the cells reported to cause neuronal dysfunction during AD. Dietary intake of polyphenols is known to attenuate the progression of the disease by showing strong potential to tackle the alterations and reduce the risk of AD by reversing the cognitive deficits. A large number of polyphenolic compounds showing promising results against AD pathologies have been identified and described in the past decade. Many efforts have been made to unravel the molecular mechanisms and the specific interactions of polyphenols with their targets in the pathway. This review focuses on the therapeutic potential and promising role of dietary polyphenols as nutraceuticals to combat AD.
Subject(s)
Alzheimer Disease/diet therapy , Flavonoids/therapeutic use , Alzheimer Disease/metabolism , Animals , Coumaric Acids/pharmacology , Coumaric Acids/therapeutic use , Curcumin/pharmacology , Curcumin/therapeutic use , Diet , Flavonoids/pharmacology , Humans , Research , Resveratrol , Stilbenes/pharmacology , Stilbenes/therapeutic useABSTRACT
The present was carried out to evaluate the toxicity of methanolic leaf extract of Rhizophora mucronata (MERM) under in vivo and in vitro conditions. Mutagenicity of MERM (up to 4,000 µg/plate) evaluated by Salmonella/microsome assay (TA98, TA100, TA1535 and TA1538 strains), with or without metabolic activation showed no mutagenic effect in any of the tester strain. Evaluation of genotoxicity (comet assay) and cytotoxicity in PBMC revealed that MERM showed no significant difference in comet tail moment (TM) and tail scores and cytotoxicity up to 24 h respectively. In acute toxicity studies, oral administration of single doses of MERM (250-2,000 mg/kg) in Wistar rats produced neither mortality nor any noticeable changes in behavior. Hematological and biochemical parameters showed no difference, except for a significant increase in ALT and AST at the highest dose. Histopathological findings revealed hepatotoxicity and neurotoxicity at highest dose of extract. In subacute toxicity studies administration of MERM (1,000 mg/kg) for 28 consecutive days neither altered the body weight gain nor behavioral parameters. No significant change was observed in the hematological and biochemical parameters analyzed. Histopathological examination showed normal architecture suggesting no morphological disturbances. Collectively, these data demonstrate that consumption of MERM for various medicinal purpose is safe.
Subject(s)
DNA Damage/drug effects , Leukocytes, Mononuclear/drug effects , Plant Extracts/administration & dosage , Animals , Dose-Response Relationship, Drug , India , Leukocytes, Mononuclear/metabolism , Mutagenicity Tests , Plant Extracts/toxicity , Rats , Rhizophoraceae/chemistryABSTRACT
Eugenol, a member of the phenylpropanoids class of chemical compounds, is a clear to pale yellow oily liquid extracted from certain essential oils especially from clove oil, nutmeg, cinnamon, and bay leaf. The antibacterial activity of eugenol and its mechanism of bactericidal action against Proteus mirabilis were evaluated. Treatment with eugenol at their minimum inhibitory concentration [0.125 % (v/v)] and minimum bactericidal concentration [0.25 % (v/v)] reduced the viability and resulted in complete inhibition of P. mirabilis. A strong bactericidal effect on P. mirabilis was also evident, as eugenol inactivated the bacterial population within 30 min exposure. Chemo-attractant property and the observance of highest antibacterial activity at alkaline pH suggest that eugenol can work more effectively when given in vivo. Eugenol inhibits the virulence factors produced by P. mirabilis as observed by swimming motility, swarming behavior and urease activity. It interacts with cellular membrane of P. mirabilis and makes it highly permeable, forming nonspecific pores on plasma membrane, which in turn directs the release of 260 nm absorbing materials and uptake of more crystal violet from the medium into the cells. SDS-polyacrylamide gel, scanning electron microscopy and Fourier transform infrared analysis further proves the disruptive action of eugenol on the plasma membrane of P. mirabilis. The findings reveal that eugenol shows an excellent bactericidal activity against P. mirabilis by altering the integrity of cell membrane.
Subject(s)
Anti-Infective Agents/pharmacology , Cell Membrane/drug effects , Cell Membrane/microbiology , Cross Infection , Eugenol/pharmacology , Proteus mirabilis/drug effects , Cell Membrane/metabolism , Microbial Sensitivity Tests/methods , Proteus mirabilis/physiologyABSTRACT
The cytochrome P 450 1A1 gene encoding a phase I metabolic enzyme appears to be a candidate for breast cancer risk. It is involved in the phase I detoxification of polycyclic aromatic hydrocarbons (PAHs) and 2-hydroxylation of estrogens and mammary carcinogens into 2-hydroxy catechol metabolites. Several studies have investigated polymorphisms in CYP1A1 and breast cancer risk with inconsistent results. We here carried out a population based case-control study of the CYP MspI (CYP1A1*1/M1) and Ile462Val (CYP1A1*2/M2) polymorphisms in CYP1A1 to clarify their importance in determining breast cancer susceptibility in a South Indian population. A total of 50 cases and 50 controls were genotyped for both polymorphisms. We also investigated putative interactions with exposure to pollution, radiation and intake of tobacco and CYP1A1 genotype and breast cancer risk using a case only study design. The genotype distribution of CYP1A1*1 in cancer patients was 6% for homozygous (CYP1A1 M1 [C/C], 34% for heterozygous CYP1A1 M1 [T/C] and 60% for wild type (CYP1A1 M1 [T/T] (OR: 0.583, CI-95% (0.252-1.348). The genotype distribution of M2 genotypes in patients was 24% of homozygous (CYP1A1 M2 [Val/Val], 4% for heterozygous (CYP1A1 M2 [Ile/Val] and 72% for wild type allele (CYP1A1 M2 [Ile/Ile] [OR: 0.720, CI-95% (0.606-0.856)]. Our results suggest that there is no significant correlation between CYP1A1 M1/ CYP1A1 M2 polymorphism and occurrence of breast cancer in South Indian women.
Subject(s)
Breast Neoplasms/genetics , Cytochrome P-450 CYP1A1/genetics , Alleles , Breast Neoplasms/enzymology , Case-Control Studies , Codon , Dietary Fats/adverse effects , Environmental Pollution/adverse effects , Exons , Female , Genetic Predisposition to Disease , Genotype , Heterozygote , Homozygote , Humans , India , Middle Aged , Risk Factors , Smoking/adverse effectsABSTRACT
PAHs are a ubiquitous class of environmental contaminants that have a large number of hazardous consequences on human health. An important prototype of PAHs, B(a)P, is notable for being the first chemical carcinogen to be discovered and the one classified by EPA as a probable human carcinogen. It undergoes metabolic activation to QD, which generate ROS by redox cycling system in the body and oxidatively damage the macromolecules. Hence, a variety of antioxidants have been tested as possible protectors against B(a)P toxicity. Silymarin is one such compound, which has high human acceptance, used clinically and consumed as dietary supplement around the world for its strong anti-oxidant efficacy. Silymarin was employed as an alternative approach for treating B(a)P induced damage and oxidative stress in PBMC, with an emphasis to provide the molecular basis for the effect of silymarin against B(a)P induced toxicity. PBMC cells exposed to either benzopyrene (1 microM) or silymarin (2.4 mg/ml) or both was monitored for toxicity by assessing LPO, PO, redox status (GSH/GSSG ratio), glutathione metabolizing enzymes GR and GPx and antioxidant enzymes CAT and SOD. This study also investigated the protective effect of silymarin against B(a)P induced biochemical alteration at the molecular level by FT-IR spectroscopy. Our findings were quite striking that silymarin possesses substantial protective effect against B(a)P induced oxidative stress and biochemical changes by restoring redox status, modulating glutathione metabolizing enzymes, hindering the formation of protein oxidation products, inhibiting LPO and further reducing ROS mediated damages by changing the level of antioxidant enzymes. The results suggest that silymarin exhibits multiple protections and it should be considered as a potential protective agent for environmental contaminant induced immunotoxicity.
Subject(s)
Antioxidants/pharmacology , Benzo(a)pyrene/toxicity , Glutathione/metabolism , Leukocytes, Mononuclear/drug effects , Protective Agents/pharmacology , Silymarin/pharmacology , Benzo(a)pyrene/antagonists & inhibitors , Catalase/metabolism , Cell Membrane/drug effects , Humans , Leukocytes, Mononuclear/metabolism , Lipid Peroxidation/drug effects , Oxidation-Reduction/drug effects , Oxidative Stress/drug effects , Superoxide Dismutase/metabolismABSTRACT
An electrochemical assay for sensing NO in biological systems is described in this paper. The ferrocene mediated reduction of NO, facilitated by the gold nanocomposite modified glassy carbon electrode is followed by an amperometric procedure. The analytical protocol involves the modification of a glassy carbon electrode by an overlayer of Au nanocomposites prepared through galvanic reduction. Additional overlayers can be built on the surface by repetition of the procedure. The modification leads to the decrease of the over-potential required for the analysis and results in a non-biofouling surface. Since the procedure is based on the electrochemical reduction of NO, the potential interferences from species like dopamine, ascorbic acid, etc., are overcome. The sensitivity, detection limit and response time achieved through this protocol for the modified electrode containing three Au overlayers are 0.03 nA/nM, 25.75 nM and <5 s. Analysis of NO has been carried out in real samples like liver extract, peripheral blood mononuclear cells (PBMCs) and miconazole nitrate ointment and the values obtained are comparable with that obtained by Griess analysis.
Subject(s)
Carbon/chemistry , Electrochemical Techniques/methods , Ferrous Compounds/chemistry , Gold/chemistry , Metal Nanoparticles/chemistry , Nitric Oxide/analysis , beta-Cyclodextrins/chemistry , 2-Hydroxypropyl-beta-cyclodextrin , Cell Extracts/chemistry , Dendrimers/chemistry , Electrodes , Metal Nanoparticles/ultrastructure , Metallocenes , Oxidation-ReductionABSTRACT
AIM OF THE STUDY: To evaluate the antibacterial activity of eugenol and its mechanism of bactericidal action against Salmonella typhi. MATERIALS AND METHODS: The antibacterial activity was checked by disc-diffusion method, MIC, MBC, time course assay and pH sensitivity assay. The chemo-attractant property of eugenol was verified by chemotaxis assay. The mode of action of eugenol was determined by crystal violet assay, measurement of release of 260 nm absorbing material, SDS-PAGE, FT-IR spectroscopy, AFM and SEM. RESULTS: Treatment with eugenol at their MIC (0.0125%) and MBC (0.025%) reduced the viability and resulted in complete inhibition of the organism. Eugenol inactivated Salmonella typhi within 60 min exposure. The chemo-attractant property of eugenol combined with the observed high antibacterial activity at alkaline pH favors the fact that the compound can work more efficiently when given in vivo. Eugenol increased the permeability of the membrane, as evidenced by crystal violet assay. The measurement of release of 260 nm absorbing intracellular materials, SDS-PAGE, SEM and AFM analysis confirmed the disruptive action of eugenol on cytoplasmic membrane. The deformation of macromolecules in the membrane, upon treatment with eugenol was verified by FT-IR spectroscopy. CONCLUSION: The results suggest that the antibacterial activity of eugenol against Salmonella typhi is due to the interaction of eugenol on bacterial cell membrane.
Subject(s)
Anti-Bacterial Agents/pharmacology , Eugenol/pharmacology , Salmonella typhi/drug effects , Cell Membrane/drug effects , Electrophoresis, Polyacrylamide Gel , Microbial Sensitivity Tests , Microscopy, Atomic Force , Microscopy, Electron, Scanning , Spectroscopy, Fourier Transform InfraredABSTRACT
The present study was carried out to evaluate the in vitro antioxidant properties and protective effects of silymarin (milk thistle) in human erythrocyte haemolysates against benzo(a)pyrene [B(a)P], a potent carcinogenic chemical. Protective effect of silymarin was assessed in vitro by monitoring the antioxidant enzymes and malondialdehyde in three groups of haemolysates-(I) vehicle control (II) B(a)P incubated group and (III) B(a)P co incubated with silymarin. The effects of silymarin on lipid peroxidation (LPO) and antioxidant enzymes [superoxide dismutase; SOD, catalase; CAT, glutathione peroxidase; GPx, glutathione reductase; GR and glutathione-S-transferases; GST] were assessed on haemolysates. It was observed that specific activity of antioxidant enzymes were significantly decreased and the malondialdehyde levels were elevated when haemolysates were incubated with B(a)P. The protective effect of silymarin is elucidated by the significant reversal of the antioxidant enzymes and reduction in the levels of malondialdehyde. In addition, haemolysates were incubated with B(a)P for 45 min and the B(a)P metabolite, 3-hydroxy benzo(a)pyrene (3-OH-B(a)P) was detected using HPLC. An increased level of the metabolite was detected in group II. Whereas, when haemolysates were co-incubated with silymarin, the reactive metabolite 3-OH-B(a)P was not detectable which further confirms the protective role of silymarin. Generation of 3-OH-B(a)P in group II implicates the possibility of reactive oxygen species (O2- and H2O2) production in haemolysates during cytochrome P4501A1 (CYP1A1) mediated Phase-I-metabolism. Hence, we incubated the haemolysates with exogenous reactive oxygen species H2O2 and assessed the protective role of silymarin against H2O2. From the results of our study, it was suggested that silymarin possess substantial protective effect and free radical scavenging mechanism against environmental contaminants induced oxidative stress damages.
Subject(s)
Antioxidants/pharmacology , Benzo(a)pyrene/toxicity , Erythrocytes/drug effects , Hydrogen Peroxide/toxicity , Oxidative Stress/drug effects , Silymarin/pharmacology , Catalase/metabolism , Erythrocytes/enzymology , Erythrocytes/metabolism , Glutathione Reductase/metabolism , Glutathione Transferase/metabolism , Hemoglobins/analysis , Hemolysis , Humans , Lipid Peroxidation/drug effectsABSTRACT
Silymarin is a polyphenolic plant flavonoid (a mixture of flavonoid isomers such as silibinin, isosilibinin, silidianin and silichristin) derived from Silymarin marianum that has anti-inflammatory, hepatoprotective and anticarcinogenic effects. Our earlier studies have shown that silymarin plays a protective role against the oxidative damage induced by environmental contaminants like benzo(a)pyrene in erythrocyte haemolysates. During the detoxification of these environmental contaminants, the major reactive oxygen species generated is hydrogen peroxide (H(2)O(2)). Because H(2)O(2 )can easily penetrate into the cell and cause damage to biomolecules, the protective role of silymarin was further assessed against this cytotoxic agent in vitro in erythrocyte haemolysates. The protective effect was monitored by assessing the levels of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-s-transferase, glutathione peroxidase and malondialdehyde (LPO) in three groups: vehicle control, H(2)O(2)-exposed groups and drug co-incubation group (H(2)O(2) + silymarin). The protective effect of silymarin on the non-enzymic antioxidant glutathione and haemolysis, methaemoglobin content and protein carbonyl content were also assessed. It was observed that the activities of antioxidant enzymes and glutathione were reduced and the malondialdehyde levels were elevated after H(2)O(2 )exposure. There were also alterations in haemolysis, methaemoglobin content and protein carbonyl content, whereas after the administration of silymarin, the antioxidant enzyme activities reversed to near normal with reduced malondialdehyde content and normalized haemolysis, methaemoglobin content and protein carbonyl content. The results suggest that silymarin possesses substantial protective effect and free radical scavenging mechanism against exogenous H(2)O(2)-induced oxidative stress damages, hence, can be used as a protective drug against toxicity induced by environmental contaminants.
Subject(s)
Antioxidants/pharmacology , Environmental Pollutants/toxicity , Erythrocytes/metabolism , Hydrogen Peroxide/toxicity , Reactive Oxygen Species/metabolism , Silymarin/pharmacology , Benzo(a)pyrene/toxicity , Humans , In Vitro Techniques , Oxidoreductases/metabolismABSTRACT
Allurement of herbs as health beneficial foods (physiologically functional foods) and as a source material for the development of new drugs, has led to greater furtherance in the study of herbal medicines during recent years. Plant extracts are being utilized to treat a wide variety of diseases like hepatotoxicity. Premna tomentosa is one such medicinal plant used widely in Indian ayurvedic medicine for the treatment of liver disorders. This study appraised the effectiveness of P. tomentosa leaf extract in protecting the liver against mitochondrial damage induced by acetaminophen, since mitochondrial injury has been investigated as a potential initiator of hepatotoxicity. Normal Wistar strain rats were pre-treated with P. tomentosa extract (750 mg/kg, orally) for 15 days and then intoxicated with acetaminophen (640 mg/kg, orally). Mitochondria were isolated from liver of experimental animals and assessed for the levels of lipid peroxide products, GSH and mitochondrial enzymes (isocitrate dehydrogenase, alpha-keto glutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and cytochrome-C-oxidase). The levels of Lipid peroxidation products were increased and the levels of the other assessed parameters were significantly decreased in hepatotoxicity induced animals. Whereas, the levels were brought back to normal in P. tomentosa pre-treated rats, which shows the protective effect of the extract against mitochondrial damage. Presence of anti-oxidant compound D-limonene (58%) in P. tomentosa leaves, which is known to enhance conjugation of toxic metabolites by maintaining liver GSH concentrations may explain the hepatoprotective property of the extract.
Subject(s)
Chemical and Drug Induced Liver Injury , Lamiaceae/chemistry , Liver Diseases/prevention & control , Mitochondria, Liver/drug effects , Phytotherapy , Acetaminophen , Animals , Male , Mitochondria, Liver/enzymology , Plant Extracts/pharmacology , Plant Extracts/therapeutic use , Plant Leaves/chemistry , Protective Agents/pharmacology , Protective Agents/therapeutic use , Rats , Rats, WistarABSTRACT
Hepatic injury elicits intracellular stress that leads to peroxidation of membrane lipids accompanied by alteration of structural and functional characteristics of membrane, which affect the activities of membrane-bound ATPases. The present study appraised the membrane protective effect of Premna tomentosa, a hepatoprotective drug used in Indian traditional medicine. Wistar strain rats were pre-treated with Premna tomentosa extract (750 mg/kg, orally) for 15 days, 24 h prior to administration of acetaminophen (640 mg/kg, orally). During acetaminophen intoxication, the levels of membrane-bound enzymes were significantly decreased, total ATPase (1.63-fold), Mg(2+)ATPase (1.9-fold), Ca(2+)ATPase (1.33-fold) and Na(+)K(+)ATPase (1.73-fold) which was accompanied by changes in the levels of inorganic cations N+, K+ and Ca2+. These alterations were prevented by Premna tomentosa extract pre-treatment, which shows that Premna tomentosa supplementation could exert a beneficial effect against liver injury-induced membrane damage. The potential of the plant might be credited to the presence of antioxidant compound limonene in the plant.
Subject(s)
Ca(2+) Mg(2+)-ATPase/metabolism , Chemical and Drug Induced Liver Injury/prevention & control , Liver/drug effects , Phytotherapy , Plant Extracts/pharmacology , Protective Agents/pharmacology , Sodium-Potassium-Exchanging ATPase/metabolism , Verbenaceae , Acetaminophen , Adenosine Triphosphatases/metabolism , Animals , Liver/enzymology , Male , Plant Extracts/administration & dosage , Plant Extracts/therapeutic use , Plant Leaves , Protective Agents/administration & dosage , Protective Agents/therapeutic use , Rats , Rats, WistarABSTRACT
Medicinal plants are believed to be an important source of new chemical substances with potential therapeutic effects. The research into plants with alleged folklore use as pain relievers should therefore be viewed as a fruitful and logical research strategy in the search of new analgesic drugs. In the present inquiry, antinociceptive effects of Premna tomentosa (PT) leaf extract (in methanol) were explored in experimental animals by acetic acid-induced writhing, tail flick and tail clip tests. Oral administration of PT extract at different doses (100, 200, 400 and 500 mg/kg) led to significant antinociceptive effects. The extract was also tested for hypnotic effects. Treatment with extracts at different doses (100, 200, 400 and 500 mg/kg) decreased the locomotor activity and potentiated the pentobarbitone-induced sleep time. The responses were dose-dependent. On the basis of the present finding, we can conclude that PT possesses antinociceptive and hypnotic activities.