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Therapeutic Methods and Therapies TCIM
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1.
J Tradit Complement Med ; 8(4): 483-496, 2018 Oct.
Article in English | MEDLINE | ID: mdl-30302329

ABSTRACT

Herbal medicines are known to mitigate radical induced cell damage. Hence identification and scientific validation of herbal medicines contribute to better use in Ayurvedic/Unani research. In the present study, we investigated antioxidant and anti-apoptotic properties of Convolvulus pluricaulis (C. pluricaulis). C. pluricaulis exhibited antioxidant potential evident by free radical scavenging activities. C. pluricaulis pretreatment inhibited H2O2 induced macromolecule damage such as plasmid DNA damage and AAPH induced oxidation of bovine serum albumin and lipid peroxidation of rat hepatic tissues. Further to identify the neuroprotective properties of C. pluricaulis, SHSY5Y cells were treated with H2O2 with or without pretreatment of C. pluricaulis. The C. pluricaulis pretreatment at 50 µg/ml dose exhibited 50% cell survival against 100 µM H2O2 challenge for 24 h and it also decreased the lactate dehydrogenase leakage. Further C. pluricaulis pretreatment restored and regulated the antioxidant and apoptosis markers such as SOD, CAT, p53, and caspase-3 and inhibited, reactive oxygen species generation and depolarization of the mitochondrial membrane. C. pluricaulis possess a high content of flavonoids and polyphenols and GC-MS and FTIR analysis showed a wide variety of compounds which may contribute to the observed effects.

2.
CNS Neurol Disord Drug Targets ; 17(9): 680-688, 2018.
Article in English | MEDLINE | ID: mdl-29938622

ABSTRACT

BACKGROUND AND OBJECTIVE: A steep rise in the incidences of neurodegenerative disorders could be the combined effect of several non-genetic factors such as increased life expectancy, environmental pollutants, lifestyle, and dietary habits, as population-level genetic change require multiple generations. Emerging evidence suggests that chronic over-nutrition induces brain metabolic stress and neuroinflammation, and are individually known to promote neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). Although the association of metabolic disorders such as diabetes, hypertension, dyslipidemia, and atherosclerosis with the dietary habits is well known, neuronal implications of diet and nutritional factors is still in its infancy. Transcriptomics and proteomics-based studies support the view that nutraceuticals target multiple neuroprotective pathways in a slow but effective manner without causing severe adverse effects, and may represent the future of tackling neurodegenerative disorders. CONCLUSION: In this article we i) review the diet/dietary supplement connection with brain metabolic stress and neuroinflammation and ii) summarize current knowledge of the effects of nutraceuticals on neurodegenerative disorders.


Subject(s)
Brain/physiopathology , Dietary Supplements , Encephalitis/pathology , Nutrients/metabolism , Stress, Physiological/physiology , Animals , Brain/metabolism , Encephalitis/therapy , Humans
3.
Metab Brain Dis ; 33(5): 1533-1549, 2018 10.
Article in English | MEDLINE | ID: mdl-29934858

ABSTRACT

Nardostachys jatamansi has profound applications against pharmacological interventions and is categorized as a hypno-sedative drug according to Ayurveda. In the present study probable mechanism of anxiolytic action of Nardostachys jatamansi extract (NJE) was studied using behavioral anxiolytic tests (Elevated plus maze, Open field test, Light dark box test, and Vogel's conflict test) in mice. Mice were treated orally with NJE (250 mg/kg) for 3, 7 and 14 days or diazepam (1 mg/kg) followed by behavioral assessment and estimation of monoamine neurotransmitters, GABA, and antioxidant enzymes. Treatment of mice for 7 days caused an increase in time spent in open arms in elevated plus maze, number of line crossings in open field test, increased time spent in lit compartment of light-dark box test, an increase in number of licks made and shocks accepted in Vogel's conflict test, with results comparable to diazepam and this treatment also caused a significant increase in monoamine neurotransmitters and GABA in brain and tissue antioxidant parameters. Co-treatment of NJE with flumazenil (GABA-benzodiazepine antagonist; 0.5 mg/kg i.p) or picrotoxin (GABAA gated chloride channel blocker; 1 mg/kg i.p) caused a blockage/antagonised anxiolytic actions of NJE by causing a significant reduction in time spent in open arms of elevated plus maze, an decrease in number of line crossing in open field test and also number of shocks and licks accepted in Vogel's conflict test. Further, NJE was radiolabelled with technetium99m at their hydroxyl groups following which purity as well as in vivo and in vitro stability of radiolabelled formulations was evaluated. The blood kinetics and in vivo bio-distribution studies were carried out in rabbits and mice respectively. Labeled formulation was found to be stable in vitro (96 to 93% stability) and in vivo (96 to 92% stability). The labeled compound was cleared rapidly from blood (within 24 h) and accumulated majorly in kidneys (11.65 ± 1.33), liver (6.07 ± 0.94), and blood (4.03 ± 0.63) after 1 h. However, a small amount was observed in brain (0.1 ± 0.02) probably because of its inability to cross blood-brain barrier. These results highlight biodistribution pattern of NJE, and also indicated that a 7-day treatment with NJE produced significant anxiolytic effects in mice and also a significant increase in brain monoamine and GABA neurotransmitter levels and suggests that anxiolytic effects of NJE are primarily and plausibly mediated by activating GABAergic receptor complex.


Subject(s)
Anti-Anxiety Agents/pharmacokinetics , Herb-Drug Interactions/physiology , Hypnotics and Sedatives/pharmacokinetics , Nardostachys/chemistry , Plant Extracts/pharmacokinetics , Receptors, GABA-A/metabolism , Animals , Anti-Anxiety Agents/administration & dosage , Anti-Anxiety Agents/pharmacology , Antioxidants/metabolism , Anxiety/drug therapy , Behavior, Animal/drug effects , Benzodiazepines/metabolism , Biogenic Monoamines/metabolism , Brain/diagnostic imaging , Diazepam/administration & dosage , Diazepam/pharmacology , Female , Flumazenil/pharmacology , GABA Antagonists/pharmacology , GABA Modulators/pharmacology , Hypnotics and Sedatives/administration & dosage , Hypnotics and Sedatives/pharmacology , Male , Maze Learning/drug effects , Mice , Phytotherapy , Picrotoxin/pharmacology , Plant Extracts/administration & dosage , Plant Extracts/pharmacology , Rabbits , Radionuclide Imaging , Tissue Distribution
4.
Biomed Pharmacother ; 91: 191-201, 2017 Jul.
Article in English | MEDLINE | ID: mdl-28458157

ABSTRACT

Elleteria repens is a large cardamom used in the culinary preparations. In the present study, we have evaluated in vitro antioxidant and free radical scavenging activities E. repens hexane extract (ERH) exhibited DPPH and metal chelating activity with IC50 values of 464±28.3µg/ml, 199±7.2µg/ml whereas the reducing power and antioxidant activities are found to be 289±14.6 AAE/mg, 468±22.7 GAE/mg. The observed antioxidant activities could be correlated with metabolites such as polyphenol, flavonoid, and terpenoid group of compounds identified in hexane fraction of E. repens by 4D GCXGC TOF-MS. Further ERH was evaluated for its protective properties against macromolecules such as DNA, protein and lipid damage. The extract showed protection against H2O2 induced DNA damage and inhibited AAPH induced protein oxidation and lipid peroxidation. Moreover, ERH administration to rats at 50 and 100mg/kg inhibited carrageenan-induced paw edema, and down-regulated cytokines such as COX-2, IL-6, and TNF-α and inhibited i-NOS mediated NO generation. E. repens also exhibited antioxidant effects by restoring SOD, catalase, GSH levels and inhibited lipid peroxidation in carrageenan challenged rats. Overall, the results suggest that E. repens may be useful in combating inflammation and oxidative stress.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Antioxidants/pharmacology , Elettaria/chemistry , Mass Spectrometry/methods , Phytochemicals/pharmacology , Animals , Biomarkers/metabolism , DNA Damage , Diclofenac/pharmacology , Flavonoids/analysis , Free Radical Scavengers/pharmacology , Interleukin-6/metabolism , Lipid Peroxidation/drug effects , Male , Nitric Oxide/biosynthesis , Oxidation-Reduction , Phenols/analysis , Plant Extracts/pharmacology , Prostaglandin-Endoperoxide Synthases/metabolism , Rats, Wistar , Tumor Necrosis Factor-alpha/metabolism
5.
Biomed Pharmacother ; 91: 1-12, 2017 Jul.
Article in English | MEDLINE | ID: mdl-28433747

ABSTRACT

Smoke induced oxidative stress is known to cause various cancers and associated health problems including lung cancer. Herbal extracts have been reported as antioxidant supplements which attenuate free radical induced oxidative damage of tissues, among which Ocimum sanctum has been reported as the elixir of life due to its innumerable health benefits. In the present study, we investigated the protective effect of O. sanctum against cracker smoke induced lung and brain tissue damage. The results of the study demonstrate that O. sanctum regulates the hematological and serum biochemical parameters such as RBC, WBC, blood urea nitrogen and creatinine kinase. O. sanctum supplementation inhibited oxidative stress as analyzed by SOD, CAT enzyme levels and i-NOS, HSP-70 protein expression. O. sanctum administration also regulated neurotransmitter levels, such as serotonin, dopamine, and regulated acetylcholine esterase levels which play a vital role in neuronal function. Further O. sanctum treatment also preserved the morphology of lung and brain tissues of smoke stress induced rats as observed by histopathology and transmission electron microscope analysis. The biodistribution of O. sanctum was showed its accumulation in key tissues such as kidney, liver, lungs and heart. The LC-ESI-MS/MS analysis of O. sanctum showed the presence of polyphenols, flavonoids and fatty acids which might be responsible for the observed anti-stress effects.


Subject(s)
Lung/pathology , Neurons/pathology , Ocimum sanctum/chemistry , Protective Agents/pharmacology , Smoke/adverse effects , Spectrometry, Mass, Electrospray Ionization/methods , Tandem Mass Spectrometry/methods , Acetylcholinesterase/metabolism , Animals , Biomarkers/blood , Brain/drug effects , Brain/pathology , Caspase 3/metabolism , Gas Chromatography-Mass Spectrometry , HSP70 Heat-Shock Proteins/metabolism , Lipid Peroxidation/drug effects , Lung/drug effects , Lung/ultrastructure , Male , Metabolome , Neurons/drug effects , Neurotransmitter Agents/metabolism , Nitric Oxide/biosynthesis , Nitric Oxide Synthase Type II/metabolism , Oxidative Stress/drug effects , Plant Extracts/chemistry , Plant Extracts/pharmacokinetics , Plant Extracts/pharmacology , Protective Agents/chemistry , Protective Agents/pharmacokinetics , Rats, Wistar , Tissue Distribution/drug effects
6.
Physiol Behav ; 175: 56-65, 2017 06 01.
Article in English | MEDLINE | ID: mdl-28351559

ABSTRACT

Hypobaric hypoxia leads to decrease in cellular oxygen content which subsequently damages the hippocampus with an increase in brain oxidative stress and impairs the memory of the individual. In the present study, we have evaluated the cognitive impairment modulating activity of total oligomeric flavonoids fraction of Cyperus rotundus (TOF) in Sprague Dawley rats. The rats were trained for memory activity for a period of 7days followed by 7days exposure to 25,000ft. altitude and the spatial reference memory was evaluated. Behavioral analysis of the rats by Morris water maze experiment showed that TOF supplementation enhanced the spatial reference memory activity of the rats exposed to hypobaric hypoxia. The decrease in antioxidant status of the animals exposed to hypoxia was restored with TOF supplementation. The increase in ROS, lipid peroxidation products and protein carbonyls of the hippocampus was significantly decreased in animals with TOF administration. The histological assessment of the pyramidal cells of the hippocampus of hypoxia-exposed animals showed nuclear damage and TOF supplementation prevented nuclear damage. TOF administration suppressed hypoxia-induced increase in serotonin, dopamine, and norepinephrine. GABA and Ach levels were decreased by hypoxia which was prevented by TOF supplementation. The increase in GFAP, HIF-1α and VEGF expression in CA3 region of the hippocampus in hypoxia-exposed rats was decreased in TOF administered rats. Taken together, TOF extract ameliorates hypobaric hypoxia induced memory impairment and neurodegeneration in hippocampus through its anti-stress effects.


Subject(s)
Cognition Disorders/drug therapy , Cognition Disorders/etiology , Cyperus/chemistry , Flavonoids/therapeutic use , Hypoxia/complications , Plant Extracts/therapeutic use , Acetylcholinesterase/metabolism , Animals , Disease Models, Animal , Dose-Response Relationship, Drug , Glutathione/metabolism , L-Lactate Dehydrogenase/metabolism , Lipid Peroxidation/drug effects , Male , Maze Learning/drug effects , Mental Recall/drug effects , Neurotransmitter Agents/metabolism , Nitrites/metabolism , Protein Carbonylation/drug effects , Rats , Rats, Sprague-Dawley
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