Neuroprotective Effects of Medicinal Plants in Cerebral Hypoxia and Anoxia: A Systematic Review

2020 ◽  
Vol 10 (5) ◽  
pp. 550-565
Author(s):  
Nasibeh Amirzargar ◽  
Saeid Heidari-Soureshjani ◽  
Qian Yang ◽  
Saber Abbaszadeh ◽  
Mojtaba Khaksarian
Keyword(s):  
Medicinal Plants ◽  
Protein Tyrosine Kinase ◽  
Scientific Information ◽  
Hypoxia Inducible Factor ◽  
Cerebral Hypoxia ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Necrosis Factor Alpha ◽  
Expression Of Genes ◽  
Inhibit Lipid Peroxidation

Background: Hypoxia and anoxia are dangerous and sometimes irreversible complications in the central nervous system (CNS), which in some cases lead to death. Objective: The aim of this review was to investigate the neuroprotective effects of medicinal plants in cerebral hypoxia and anoxia. Methods: The word hypox*, in combination with some herbal terms such as medicinal plant, phyto* and herb*, was used to search for relevant publications indexed in the Institute for Scientific Information (ISI) and PubMed from 2000-2019. Results: Certain medicinal plants and herbal derivatives can exert their protective effects in several ways. The most important mechanisms are the inhibition of inducible nitric oxide synthase (iNOS), production of NO, inhibition of both hypoxia-inducible factor 1α and tumor necrosis factor-alpha activation, and reduction of extracellular glutamate, N-Methyl-D-aspartic and intracellular Ca (2+). In addition, they have an antioxidant activity and can adjust the expression of genes related to oxidant generation or antioxidant capacity. These plants can also inhibit lipid peroxidation, up-regulate superoxide dismutase activity and inhibit the content of malondialdehyde and lactate dehydrogenase. Moreover, they also have protective effects against cytotoxicity through down-regulation of the proteins that causes apoptosis, anti-excitatory activity, inhibition of apoptosis signaling pathway, reduction of pro-apoptotic proteins, and endoplasmic reticulum stress that causes apoptosis during hypoxia, increasing anti-apoptotic protein, inhibition of protein tyrosine kinase activation, decreasing proteases activity and DNA fragmentation, and upregulation of mitochondrial cytochrome oxidase. Conclusion: The results indicated that medicinal plants and their compounds mainly exert their neuroprotective effects in hypoxia via regulating proteins that are related to antioxidant, anti-apoptosis and anti-inflammatory activities.

A Review on Possible Therapeutic Effect of Nigella sativa and Thymoquinone in Neurodegenerative Diseases

2018 ◽  
Vol 17 (6) ◽  
pp. 412-420 ◽  
Author(s):  
Saeed Samarghandian ◽  
Tahereh Farkhondeh ◽  
Fariborz Samini
Keyword(s):  
Medicinal Plants ◽  
Neurodegenerative Diseases ◽  
Nigella Sativa ◽  
Neurological Diseases ◽  
Volatile Oil ◽  
Protective Effects ◽  
Active Components ◽  
Neuroprotective Effects ◽  
Black Cumin ◽  
Main Components

Background & Objective: Medicinal plants have attracted great attention in the recent years and is increasingly applied instead of the chemical drugs. Several documents showed that herbal medicine traditionally and clinically applied in the cure and prevention of several diseases. In the recent years, different medicinal plants and their main components have been chosen in neurological therapy. The less toxic effects, availability, and lower price of medicinal plants versus synthetic substances make them as excellent and simple selection in the treatment of nervous diseases. Nigella sativa (N. Sativa) L. (Ranunculaceae), well recognized as black cumin, has been utilized as a medicinal plant that has a strong traditional background. Thymoquinone (TQ) is one of the main active components of the volatile oil of N. sativa seeds and most effects and actions of N. Sativa are mainly related to TQ. The several pharmacological properties of N. sativa and TQ have been found, for example; anti-tumor, anti-microbial, anti-histaminic, immunomodulatory, anti-inflammatory, and anti-oxidant effects. Many reviews have investigated this valuable plant and its components, but none of them focused on their neuroprotective effects. Therefore, the aim of the present review was to show comprehensive and neuropharmacological properties of N. sativa and TQ. In this review, various studies on scientific databases regarding the effects of N. sativa and TQ in neurological diseases have been introduced. Studies on the neuroprotective effects of N. sativa and TQ which were published between1979 and 2018, were searched using various databases. The results of these studies showed that N. sativa and TQ have the protective effects against neurodegenerative diseases, including; Alzheimer, depression, encephalomyelitis, epilepsy, ischemia, Parkinson, and traumatic brain injury have been discussed in the cell lines and experimental animal models. Although there are many studies indicating the beneficial actions of this plant in the nervous system, the number of research projects relating to the human reports is rare. Conclusion: Therefore, better designed clinical trials in humans are needed to confirm these effects.

scholarly journals Phytotherapy for seizure: An overview of the most important indigenous Iranian medicinal plants with anticonvulsant properties

2019 ◽  
Vol 6 (4) ◽  
pp. 367-372
Author(s):  
Behrooz Farzan ◽  
Somayeh Shahsavari ◽  
Saber Abbaszadeh ◽  
Hassan Teimouri
Keyword(s):  
Medicinal Plants ◽  
Scientific Information ◽  
Epileptic Seizures ◽  
Review Article ◽  
Anticonvulsant Effect ◽  
Protective Effects ◽  
Congenital Diseases ◽  
Search Terms ◽  
Heracleum Persicum ◽  
Lavandula Officinalis

The statistics show that more than fifty million people worldwide suffer from seizure and epilepsy, and most of them are resistant to antiepileptic drugs. The causes of seizure attacks are different, including various diseases of the nervous system, infections, tumors, brain trauma, congenital diseases, fever, toxicity and metabolic factors. Currently, drugs such as phenytoin, phenobarbital, carbamazepine, valproic acid and diazepam are used to treat epileptic seizures, which in turn lead to side effects. Studies have shown that the use of natural and herbal antiseptic agents has beneficial and protective effects. In this review article, the most important indigenous Iranian medicinal plants used to treat seizures are reported. Information to conduct this review article has been obtained using the search terms seizure, neurological lesion, phytotherapy, Iran, medicinal plants, extracts and essential oils to retrieve articles indexed in databases such as Scopus, Scientific Information Database, Magiran, Google Scholar and other Persian databases. The relevant articles were further reviewed for medicinal plants with anticonvulsant properties. Based on the results, medicinal plants such as Peganum harmala, Lavandula officinalis, Matricaria chamomilla, Tanacetum sonbolii, Launaea acanthodes, Ocimum basilicum, Salvia sahendica, Ruta graveolens, Elaeagnus angustifolia, Ziziphora tenuior, Heracleum persicum and Scrophularia striata are among the most important medicinal plants in Iran with anticonvulsant effect.

scholarly journals Role of endocannabinoid CB1 receptors in Streptozotocin-induced uninephrectomised Wistar rats in diabetic nephropathy

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Jayarami Reddy Medapati ◽  
Deepthi Rapaka ◽  
Veera Raghavulu Bitra ◽  
Santhosh Kumar Ranajit ◽  
Girija Sankar Guntuku ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Morphological Changes ◽  
Serum Levels ◽  
Cb1 Receptors ◽  
Protective Effects ◽  
Renal Hypertrophy ◽  
Necrosis Factor Alpha

Abstract Background The endocannabinoid CB1 receptor is known to have protective effects in kidney disease. The aim of the present study is to evaluate the potential agonistic and antagonistic actions and to determine the renoprotective potential of CB1 receptors in diabetic nephropathy. The present work investigates the possible role of CB1 receptors in the pathogenesis of diabetes-induced nephropathy. Streptozotocin (STZ) (55 mg/kg, i.p., once) is administered to uninephrectomised rats for induction of experimental diabetes mellitus. The CB1 agonist (oleamide) and CB1 antagonist (AM6545) treatment were initiated in diabetic rats after 1 week of STZ administration and were given for 24 weeks. Results The progress in diabetic nephropathy is estimated biochemically by measuring serum creatinine (1.28±0.03) (p < 0.005), blood urea nitrogen (67.6± 2.10) (p < 0.001), urinary microprotein (74.62± 3.47) (p < 0.005) and urinary albuminuria (28.31±1.17) (p < 0.0001). Renal inflammation was assessed by estimating serum levels of tumor necrosis factor alpha (75.69±1.51) (p < 0.001) and transforming growth factor beta (8.73±0.31) (p < 0.001). Renal morphological changes were assessed by estimating renal hypertrophy (7.38± 0.26) (p < 0.005) and renal collagen content (10.42± 0.48) (p < 0.001). Conclusions From the above findings, it can be said that diabetes-induced nephropathy may be associated with overexpression of CB1 receptors and blockade of CB1 receptors might be beneficial in ameliorating the diabetes-induced nephropathy. Graphical abstract

scholarly journals Myeloid HIF1α Is Involved in the Extent of Orthodontically Induced Tooth Movement

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 796
Author(s):  
Christian Kirschneck ◽  
Nadine Straßmair ◽  
Fabian Cieplik ◽  
Eva Paddenberg ◽  
Jonathan Jantsch ◽  
...  
Keyword(s):  
Bone Density ◽  
Periodontal Ligament ◽  
Tooth Movement ◽  
Hypoxia Inducible Factor ◽  
Myeloid Cells ◽  
Orthodontic Tooth Movement ◽  
Periodontal Ligament Fibroblasts ◽  
Expression Of Genes ◽  
Periodontal Bone Loss

During orthodontic tooth movement, transcription factor hypoxia-inducible factor 1α (HIF1α) is stabilised in the periodontal ligament. While HIF1α in periodontal ligament fibroblasts can be stabilised by mechanical compression, in macrophages pressure application alone is not sufficient to stabilise HIF1α. The present study was conducted to investigate the role of myeloid HIF1α during orthodontic tooth movement. Orthodontic tooth movement was performed in wildtype and Hif1αΔmyel mice lacking HIF1α expression in myeloid cells. Subsequently, µCT images were obtained to determine periodontal bone loss, extent of orthodontic tooth movement and bone density. RNA was isolated from the periodontal ligament of the control side and the orthodontically treated side, and the expression of genes involved in bone remodelling was investigated. The extent of tooth movement was increased in Hif1αΔmyel mice. This may be due to the lower bone density of the Hif1αΔmyel mice. Deletion of myeloid Hif1α was associated with increased expression of Ctsk and Acp5, while both Rankl and its decoy receptor Opg were increased. HIF1α from myeloid cells thus appears to play a regulatory role in orthodontic tooth movement.

Neuroprotective Effects of a GLP-2 Analogue in the MPTP Parkinson’s Disease Mouse Model

2021 ◽  
pp. 1-15
Author(s):  
Zijuan Zhang ◽  
Li Hao ◽  
Ming Shi ◽  
Ziyang Yu ◽  
Simai Shao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Mouse Model ◽  
Neurodegenerative Disorder ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Expression Levels ◽  
Dual Agonist

Background: Glucagon-like peptide 2 (GLP-2) is a peptide hormone derived from the proglucagon gene expressed in the intestines, pancreas and brain. Some previous studies showed that GLP-2 improved aging and Alzheimer’s disease related memory impairments. Parkinson’s disease (PD) is a progressive neurodegenerative disorder, and to date, there is no particular medicine reversed PD symptoms effectively. Objective: The aim of this study was to evaluate neuroprotective effects of a GLP-2 analogue in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) PD mouse model. Methods: In the present study, the protease resistant Gly(2)-GLP-2 (50 nmol/kg ip.) analogue has been tested for 14 days by behavioral assessment, transmission electron microscope, immunofluorescence histochemistry, enzyme-linked immunosorbent assay and western blot in an acute PD mouse model induced by MPTP. For comparison, the incretin receptor dual agonist DA5-CH was tested in a separate group. Results: The GLP-2 analogue treatment improved the locomotor and exploratory activity of mice, and improved bradykinesia and movement imbalance of mice. Gly(2)-GLP-2 treatment also protected dopaminergic neurons and restored tyrosine hydroxylase expression levels in the substantia nigra. Gly(2)-GLP-2 furthermore reduced the inflammation response as seen in lower microglia activation, and decreased NLRP3 and interleukin-1β pro-inflammatory cytokine expression levels. In addition, the GLP-2 analogue improved MPTP-induced mitochondrial dysfunction in the substantia nigra. The protective effects were comparable to those of the dual agonist DA5-CH. Conclusion: The present results demonstrate that Gly(2)-GLP-2 can attenuate NLRP3 inflammasome-mediated inflammation and mitochondrial damage in the substantia nigra induced by MPTP, and Gly(2)-GLP-2 shows neuroprotective effects in this PD animal model.

Protective effects of astaxanthin on lipopolysaccharide-induced inflammation in bovine endometrial epithelial cells†

2019 ◽  
Vol 102 (2) ◽  
pp. 339-347 ◽  
Author(s):  
Fa-Chun Wan ◽  
Chen Zhang ◽  
Qing Jin ◽  
Chen Wei ◽  
Hong-Bo Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
B Cell Lymphoma ◽  
Resistant Bacteria ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Antibiotic Resistant ◽  
Injury Treatment ◽  
Endometrial Epithelial Cells

Abstract Astaxanthin (AST), a natural antioxidant carotenoid, has been shown to exert anti-inflammatory effects. However, to our knowledge, no study has specifically addressed the potential protective effects of AST against bovine endometritis. The purpose of this study was to examine whether treatment with AST could protect endometrial epithelial cells against lipopolysaccharide (LPS)-induced inflammatory injury. Treatment of bovine endometrial (BEND) epithelial cell line with AST reduced LPS-induced production of interleukin-6 and tumor necrosis factor-alpha, increased the cellular activity of superoxide dismutase and catalase, decreased the proportion of apoptotic cells, and promoted the production of insulin-like growth factor and epithelial growth factor. The effects of AST were mediated through the downregulation of B-cell lymphoma 2 (Bcl-2) associated X, apoptosis regulator (Bax), and cleaved caspase-3 and through the upregulation of Bcl-2. Moreover, AST significantly increased the expression of the tight junction proteins (TJP) claudin, cadherin-1, and TJP1, which play an essential role in the maintenance of host endometrial defense barrier against pathogen infection. Collectively, these results demonstrated that treatment with AST protected against oxidative stress, prevented cell apoptosis, promoted BEND cells viability, and increased the production of growth factors, in addition to activating the endometrial defense barrier. Therefore, AST is a promising therapeutic agent for the prevention and treatment of endometritis. This finding is of utmost importance in the present times when the excessive use of antibiotics has resulted in the development of antibiotic-resistant bacteria.

scholarly journals Humanin is an endogenous activator of chaperone-mediated autophagy

2017 ◽  
Vol 217 (2) ◽  
pp. 635-647 ◽  
Author(s):  
Zhenwei Gong ◽  
Inmaculada Tasset ◽  
Antonio Diaz ◽  
Jaime Anguiano ◽  
Emir Tas ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Heat Shock Protein 90 ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Selective Degradation ◽  
Cytosolic Side ◽  
Chaperone Mediated Autophagy

Chaperone-mediated autophagy (CMA) serves as quality control during stress conditions through selective degradation of cytosolic proteins in lysosomes. Humanin (HN) is a mitochondria-associated peptide that offers cytoprotective, cardioprotective, and neuroprotective effects in vivo and in vitro. In this study, we demonstrate that HN directly activates CMA by increasing substrate binding and translocation into lysosomes. The potent HN analogue HNG protects from stressor-induced cell death in fibroblasts, cardiomyoblasts, neuronal cells, and primary cardiomyocytes. The protective effects are lost in CMA-deficient cells, suggesting that they are mediated through the activation of CMA. We identified that a fraction of endogenous HN is present at the cytosolic side of the lysosomal membrane, where it interacts with heat shock protein 90 (HSP90) and stabilizes binding of this chaperone to CMA substrates as they bind to the membrane. Inhibition of HSP90 blocks the effect of HNG on substrate translocation and abolishes the cytoprotective effects. Our study provides a novel mechanism by which HN exerts its cardioprotective and neuroprotective effects.

scholarly journals Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

2017 ◽  
Vol 68 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Mahmoud M. Said ◽  
Marwa M. Abd Rabo
Keyword(s):  
Total Antioxidant Status ◽  
Basal Diet ◽  
Acetylcholinesterase Activity ◽  
Aluminium Chloride ◽  
Neuroprotective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Male Wistar Rats

AbstractAluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000 μg g-1eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1protein) and 5-HT (2.13±0.27 ng mg-1tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1protein) and Casp-3 (3.80±0.37 ng mg-1protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

Neuroprotective effects of macamide from maca (Lepidium meyenii Walp.) on corticosterone-induced hippocampal impairments through anti-inflammatory, neurotrophic, and synaptic protection properties

2021 ◽  
Author(s):  
Zejun Yu ◽  
Dong Li ◽  
Shengbing Zhai ◽  
Hang Xu ◽  
Liu Hao ◽  
...  
Keyword(s):  
Subcutaneous Injection ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Lepidium Meyenii ◽  
Anti Inflammatory

The present study aims to investigate protective effects of N-(3-methoxybenzyl)-(9Z,12Z,15Z)-oc tadecatrienamide (M 18:3) on corticosterone-induced neurotoxicity. A neurotoxic model was established by subcutaneous injection of corticosterone (40 mg per kg·bw)...

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