Neuroprotective properties of Valeriana officinalis extracts (original) (raw)
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Pharmacologia, 2015
Background: Traditionally, the plant Valeriana officinalis is used for various diseases via headaches, anxiety, high blood pressure, menstrual cramps, epilepsy including neuronal disorders. Objective: To evaluate the neuroprotective activity of Valeriana officinalis against global cerebral ischemia induced oxidative stress in rat. Materials and methods: Neuroprotective activity was carried out by oxidative stress on Sprague-Dawley rats. Evaluation of cerebroprotective activity of Valeriana officinalis (100, 200 and 400 mg kgG 1 oral doses) was carried out by using, the global cerebral ischemia induced by Bilateral Carotid Artery (BCA) occlusion for 30 min, followed by 24 h reperfusion. The antioxidant enzymatic and non-enzymatic levels were estimated along with cerebral infarction area, blood brain barrier disruption and histophathological studies. Results: The ethanol extract of Valeriana officinalis showed neuroprotective activity by significant decrease in lipid peroxidation (p<0.05-p<0.01) and increase in superoxide dismutase (p<0.05), catalase, glutathione (p<0.05-p<0.001) and total thiol levels (p<0.05-p<0.01) in extract treated groups as compared to control group. Blood brain barrier disruption and cerebral infarction area was significantly reduced in extract treated groups as compared to control group and % infraction volume was reduced in ethanol extract of Valeriana officinalis treated groups (p<0.001), as compared to control group. Histopathological observation further support the potent neuroprotective activity of Valeriana officinalis. Conclusion: The ethanol extract of Valeriana officinalis showed neuroprotective activity against global cerebral ischemia induced oxidative stress in rat model.
In vitro antioxidant activity of Valeriana officinalis against different neurotoxic agents
2009
Valeriana officinalis L. (Valerian) is widely used as a traditional medicine to improve the quality of sleep. Although V. officinalis have been well documented as promising pharmacological agent; the exact mechanisms by which this plant act is still unknown. Limited literature data have indicated that V. officinalis extracts can exhibit antioxidant properties against iron in hippocampal neurons in vitro. However, there is no data available about the possible antioxidant effect of V. officinalis against other pro-oxidants in brain. In the present study, the protective effect of V. officinalis on lipid peroxidation (LPO) induced by different pro-oxidant agents with neuropathological importance was examined. Ethanolic extract of valerian (0-60 lg/ml) was tested against quinolinic acid (QA); 3-nitropropionic acid; sodium nitroprusside; iron sulfate (FeSO 4) and Fe 2? /EDTA induced LPO in rat brain homogenates. The effect of V. officinalis in deoxyribose degradation and reactive oxygen species (ROS) production was also investigated. In brain homogenates, V. officinalis inhibited thiobarbituric acid reactive substances induced by all pro-oxidants tested in a concentration dependent manner. Similarly, V. officinalis caused a significant decrease on the LPO in cerebral cortex and in deoxyribose degradation. QA-induced ROS production in cortical slices was also significantly reduced by V. officinalis. Our results suggest that V. officinalis extract was effective in modulating LPO induced by different pro-oxidant agents. These data may imply that V. officinalis extract, functioning as antioxidant agent, can be beneficial for reducing insomnia complications linked to oxidative stress.
Traditional Medicine Research, 2022
Background: Inflammation and damage to neurons and other cells in the nervous system can cause disorders of the central nervous system. Microglial cells are activated by pathogen infection and injury to release nitric oxide. Valerian (Valeriana officinalis) has been used as a sedative for the treatment of neurological diseases. This study evaluated inflammation of microglial cells and tumor necrosis factor α and induced nitric oxide synthetase gene expression influenced by valerian extract. Methods: Microglial cells were isolated from mice. Lipopolysaccharide (1 ng/mL) was used to induce inflammation and nitric oxide production in cells for an hour. The inflamed cells were then treated with different concentrations (0.1, 0.5, 2.5, 20, and 50 μL/mL) of valerian alcoholic extract for 1 and 24 h. nitric oxide production and tumor necrosis factor α and induced nitric oxide synthetase gene expression were determine by Griess assay and real-time polymerase chain reaction, respectively. Results: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed no toxicity in several concentrations of the valerian extract. In addition, concentrations from 0.1 to 2.5 μL/mL significantly reduced inflammation and nitric oxide production in mouse microglial cells to levels observed in control samples. Furthermore, tumor necrosis factor α and induced nitric oxide synthetase gene expression decreased when 2.5 μL/mL extract was used. Conclusion: Based on these results, it can be concluded that 2.5 μL/mL valerian alcoholic extract is effective as a candidate alternative medicine for reducing inflammation and nitric oxide production and consequently, the inflammatory symptoms of neurodegeneration.
American Journal of Phytomedicine and Clinical Therapeutics, 2014
Objectives: To investigate the neuroprotective efficacy of Valeriana wallichii DC rhizome extract against 1-methyl-4-phenlypyridinium (MPP + ) and tunicamycin induced cell death. Methods: The 50% methanolic extract of V. wallichii rhizome (VWE) was evaluated for free radical scavenging properties. Cell viability analysis and IC50 determination for VWE in SH-SY5Y neuroblastoma cell line was performed by MTT assay. The neuroprotective efficacy of VWE in SH-SY5Y cells against the damages induced by the neurotoxin, MPP + and the endoplasmic reticulum stress inducer, tunicamycin was assessed by MTT assay and by morphological analysis with phase contrast microscope. MTT assay was performed using 3 different concentrations (0.1, 0.5 and 1 mg/mL) of VWE that were added at 0, 8 and 16 h post MPP + and tunicamycin treatment. Results: VWE showed good free radical scavenging properties. From the cell viability analysis the IC50 value of VWE was calculated as 2.207 mg/mL in SH-SY5Y cells. In MPP + treated cells 0.5mg and 1mg/mL concentrations of VWE brought significant improvement in cell viability at 0h, while at 8h and 16h post MPP + treatment the effect was significant at 1mg/ml concentration. VWE exhibited significant protective effect in tunicamycin treated cells only at 0h but not at 8h and 16h post treatment. MPP + and tunicamycin induced cell shrinkage and condensation were inhibited by treatment with 1mg/mL of VWE. Conclusions: The present work is the first study that sheds light on the cytoprotective effect of Valeriana wallichii DC rhizome and provides lead for identification and isolation of novel drugs for various neurodegenerative diseases
Pharmaceuticals
Alzheimer’s disease (AD) is a neurodegenerative disorder whose pathophysiology includes the abnormal accumulation of proteins (e.g., β-amyloid), oxidative stress, and alterations in neurotransmitter levels, mainly acetylcholine. Here we present a comparative study of the effect of extracts obtained from endemic Argentinian species of valerians, namely V. carnosa Sm., V. clarionifolia Phil. and V. macrorhiza Poepp. ex DC from Patagonia and V. ferax (Griseb.) Höck and V. effusa Griseb., on different AD-related biological targets. Of these anxiolytic, sedative and sleep-inducing valerians, V. carnosa proved the most promising and was assayed in vivo. All valerians inhibited acetylcholinesterase (IC50 between 1.08–12.69 mg/mL) and butyrylcholinesterase (IC50 between 0.0019–1.46 mg/mL). They also inhibited the aggregation of β-amyloid peptide, were able to chelate Fe2+ ions, and exhibited a direct relationship between antioxidant capacity and phenolic content. Moreover, V. carnosa was ab...
Pharmacognosy Journal, 2018
Objective: Alzheimer's disease (AD) is the most common cause of dementia in worldwide, treatment options is extremely limited and costly. The present study was conducted to investigate and validate the traditional claim of Valeriana wallichii on scopolamine treated rats as an AD model. Methods: The Valeriana wallichii rhizome ethanol extract (25 mg/kg/day) was administered daily along with scopolamine for a period of 14 days following which the elevated plus maze test were performed to assess learning and memory. Rats treated with scopolamine or vehicle only were also included in the experiment. Result: The study demonstrate that scopolamine treatment resulted in learning and memory deficits which were partially and significantly ameliorated by the Valeriana wallichii rhizome ethanol extract. Conclusion: The study demonstrates the ability of the Valeriana wallichii rhizome ethanol extract to reverse scopolamine-induced learning and memory deficits in rats.
Neurochemical Research, 2009
Parkinson 0 s disease (PD) is one of the most important neurodegenerative worldwide disorders. The potential cytoprotective effects of aqueous extract of Valeriana officinalis on rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells were demonstrated. The cytotoxicity, cell viability and analysis of cellular morphology were performed by MTT-tetrazole (3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and phase contrast microscopy, respectively. Significant changes in the cellular morphology, and condensation of the cell body could be observed when cells were treated with 300 nM rotenone for 48 h. Three different concentrations of Valeriana officinalis extract were used (0.049, 0.098 and 0.195 mg/mL). These extracts brought about an increase of 7.0 ± 1.3%, 14.5 ± 1.3% and 14.5 ± 3.2% in cell viability. Our results indicated that neuroprotector action of the Valeriana officinalis extract provides support for later studies as they help understanding this drug for the development of cytoprotective various therapies in PD.
Herbal preparations prevent beta-amyloid peptide induced hippocampal cell damage
2017
The aggregates of Aβ(1-40) and Aβ(1-42) peptides are considered as the pathological hallmarks of Alzheimer's disease. The present work examined the ability of several plant preparations to protect the viability of hippocampal cells in the presence of aggregated Aβ peptides. The inhibition of the viability of rat hippocampal cells by the preliminarily aggregated peptides down to 20±2.5% of control was proved. In the presence of aggregated Aβ peptides, the cell viability was saved at 51-114% of control in the medium containing the ethanol extracts from grape and sorrel leaves, rose petals, melilot, phenol glycoside and flavonoid fractions from these extracts. The DNA-comet analysis evidenced the cell integrity conserving by the extracts, but not by the phenol glycoside fraction from rose petals, which significantly protected the cell viability from aggregated Aβ(1-40) and Aβ(1-42) (IC50 = 0.2 ± 0.02 and 2.1 ± 0.7 μg/ml, respectively). Conclusion: the studied plants can be consider...
Biomedicine & Pharmacotherapy
Alzheimer's disease (AD) is a grave and prevailing neurodegenerative disease, characterized by slow and progressive neurodegeneration in different brain regions. Aluminum (Al) is a potent and widely distributed neurotoxic metal, implicated in the neuropathogenesis of AD. This study aimed to evaluate the possible neurorestorative potential of Vitis vinifera Leaves Polyphenolic (VLP) extract in alleviating aluminum chloride (AlCl 3)-induced neurotoxicity in male rats. AlCl 3 neurotoxicity induced a significant decrease in brain/serum acetylcholine (ACh) contents and serum dopamine (DA) levels, along with a significant increment of brain/serum acetylcholinesterase (AChE) activities. In addition, Al treatment resulted in significantly decreased serum levels of both total antioxidant capacity (TAC) and brain-derived neurotrophic factor (BDNF), and significantly increased serum levels of both interleukin-6 (IL-6) and total homocysteine (tHcy), as compared to control. Behavioral alterations, assessed by the T-maze test, showed impaired cognitive function. Furthermore, AD-brains revealed an increase in DNA fragmentation as evidenced by comet assay. AlCl 3 induction also caused histopathological alterations in AD-brain. Treatment of AD-rats with VLP extract (100 mg/kg body weight/day) improved neurobehavioral changes, as evidenced by the improvement in brain function, as well as, modulation of most biochemical markers, and confirmed by T-maze test, the histopathological study of the brain and comet assay. The current work indicates that the VLP extract has neuroprotective, antioxidative, anti-inflammatory, and anti-amnesic activities against AlCl 3-induced cerebral damages and neurocognitive dysfunction.