scholarly journals Evaluation of neuroprotective potential of methanolic extract of Hemidesmus indicus extract in Aβ (1-42) induced rats

2020 ◽  
Vol 11 (4) ◽  
pp. 7495-7502
Author(s):  
Swati Som ◽  
Justin Antony ◽  
Palanisamy Dhanabal S ◽  
Sivasankaran Ponnusankar
Keyword(s):  
Methanolic Extract ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Functional Decline ◽  
Treatment Protocol ◽  
Neuroprotective Activity ◽  
Pharmacological Intervention ◽  
Hemidesmus Indicus ◽  
Neurochemical Analysis ◽  
Neurobehavioral Deficits

Excessive cerebral deposition of amyloid-beta (Aβ) peptides with 40-42 amino acids are the major neuropathologic feature of Alzheimer's Disease (AD), accompanied by a progressive and functional decline in cognition. With the failing attempts in the development of new pharmacological intervention and due to suboptimal results from the existing therapies available for the treatment of AD, there is a constant hunt for a new therapeutic alternative to address this severe neurodegenerative disease. The present study aimed to investigate the neuroprotective effect of Hemidesmus indicus extract in Aβ (1-42) infused model of AD. Sporadic model of AD was achieved by intracerebroventricular (i.c.v) injection of Aβ (1-42) peptide in Wistar rats, followed by treatment with methanolic extract of H. indicus (MEHI) at 100 and 200 mg/kg for 28 days. Locomotor activity, Radial arm Maze task and Passive avoidance test were used for the assessment of neurobehavioral deficits. After completion of 28 days treatment protocol, animals were euthanized and brains were collected for neurochemical analysis. Reversal of cognitive impairment was observed by MEHI on Aβ (1-42) rats, as evidenced by improved spatial memory learning. Furthermore, MEHI attenuated Aβ (1-42) induced oxidative stress and inhibited acetylcholine esterase (AChE) activity. Collectively, these findings exhibited neuroprotective activity of MEHI by ameliorating Aβ (1-42) mediated neuronal damage, thereby can stand as a potential disease-modifying therapeutic for curbing AD pathology.

Neuroprotective Activity of the Methanolic Extract of Indigofera aspalathoides against Scopalamine induced Alzheimer's Disease in Experimental Rats

2021 ◽  
pp. 5163-5168
Author(s):  
Rajaram C. ◽  
S. Nelson Kumar ◽  
S. S. Sheeba Tabassum ◽  
Manohar R. ◽  
Sumanjali C.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traditional Medicine ◽  
Methanolic Extract ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Neuroprotective Activity ◽  
Control Group ◽  
Histological Structure ◽  
Anticancer Activities

The plant Indigofera aspalathoides is a traditional medicine with tremendous therapeutic potential which finds it use in treatment of various ailments such as antibacterial, antioxidant, anti-inflammatory, antidiabetic, and anticancer activities. There are no reports that related to the use of this plant in treating patients with Alzheimer’s disease (AD). Hence present study was aimed to scientifically evaluate the neuroprotective effect of the methanolic extract of Indigofera aspalathoides against scopalamine induced Alzheimer’s disease in experimental rats using behavioral tests like elevated plus maze, Y-maze, and rota-rod tests. In addition to this, biochemical evaluation for acetylcholinesterase activity and histopathological evaluation of brain were done. The results suggests that methanolic extract Indigofera aspalathoides (200mg/kg B.wt and 400mg/kg B.wt) used in this study shows significant improvement of various behavioral parameters like locomotion, anxiety, memory, motor integrity and coordination etc when compared to control group. MEIA inhibited brain AChE enzyme, thereby elevating Ach concentration in brain homogenate and ultimately improved memory of rats. Further, more or less normal histological structure of the hippocampus and all amyloid plaques and neurofibrillary tangles that are formed under the influence of scopolamine disappeared in the rats pretreated with MEIA (200mg/kg B.wt and 400mg/kg B.wt). It can be concluded that our results strongly support the anti-Alzheimer’s potential of the methanolic extract of the plant I.aspalathoides and its use in traditional medicine.

scholarly journals Stimulation of β2-Adrenoceptors Inhibits Apoptosis in Rat Brain after Transient Forebrain Ischemia

1998 ◽  
Vol 18 (9) ◽  
pp. 1032-1039 ◽  
Author(s):  
Yuan Zhu ◽  
Carsten Culmsee ◽  
Irina Semkova ◽  
Josef Krieglstein
Keyword(s):  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Global Ischemia ◽  
Neuroprotective Activity ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Dna Laddering

We have previously demonstrated that the neuroprotective effect of the β2-adrenoceptor agonist clenbuterol in vitro and in vivo was most likely mediated by an increased nerve growth factor (NGF) expression. In the present study, we examined whether clenbuterol was capable of inhibiting apoptosis caused by ischemia. Transient forebrain ischemia was performed in male Wistar rats (300 to 350 g) by clamping both common carotid arteries and reducing the blood pressure to 40 mm Hg for 10 minutes. Clenbuterol(0.1, 0.5, and 1.0 mg/kg intraperitoneally) was administered 3 hours before ischemia or immediately after ischemia. The brains were removed for histologic evaluation 7 days after ischemia. The time course of DNA fragmentation was determined 1, 2, 3 and 4 days after ischemia. Staining with terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick end-labeling (TUNEL) was used for further analysis of DNA fragments in situ 3 days after ischemia. The NGF protein was assayed by enzyme-linked immunosorbent assay. Ten-minute forebrain ischemia damaged 80% to 90% of the neurons in the hippocampal CA1 region evaluated 7 days after ischemia. Pretreatment with clenbuterol (0.5 and 1.0 mg/kg) reduced the neuronal damage by 18.1% ( P< 0.01) and 13.1% ( P < 0.05), respectively. The neuroprotective effect also was found when clenbuterol (0.5 mg/kg) was administered immediately after ischemia ( P < 0.05). The DNA laddering appeared in striatum 1 day and in hippocampus 2 days after ischemia and peaked on the third day in both regions. The DNA laddering was nearly abolished in the hippocampus and partially blocked in striatum and cortex by 0.5 mg/kg clenbuterol. These results were confirmed by TUNEL staining. Clenbuterol (0.5 mg/kg intraperitoneally) elevated the NGF protein level by 33% ( P < 0.05) in the hippocampus and 41% ( P < 0.05) in the cortex 6 hours after ischemia. Three days after ischemia, the NGF levels in these regions were no longer different between the clenbuterol-treated and control groups. This study clearly demonstrates that clenbuterol possesses a neuroprotective activity and a marked capacity to inhibit DNA degradation after global ischemia. The results suggest that clenbuterol increases NGF expression during the first hours after global ischemia and thereby protects neurons against apoptotic damage.

scholarly journals Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy

2021 ◽  
Vol 22 (9) ◽  
pp. 4667
Author(s):  
Michaela Shishmanova-Doseva ◽  
Dimitrinka Atanasova ◽  
Yordanka Uzunova ◽  
Lyubka Yoanidu ◽  
Lyudmil Peychev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Basolateral Amygdala ◽  
Neuronal Damage ◽  
Piriform Cortex ◽  
Preference Test ◽  
Neuroprotective Activity ◽  
Object Recognition Test ◽  
Beneficial Effects

Clinically, temporal lobe epilepsy (TLE) is the most prevalent type of partial epilepsy and often accompanied by various comorbidities. The present study aimed to evaluate the effects of chronic treatment with the antiepileptic drug (AED) lacosamide (LCM) on spontaneous motor seizures (SMS), behavioral comorbidities, oxidative stress, neuroinflammation, and neuronal damage in a model of TLE. Vehicle/LCM treatment (30 mg/kg, p.o.) was administered 3 h after the pilocarpine-induced status epilepticus (SE) and continued for up to 12 weeks in Wistar rats. Our study showed that LCM attenuated the number of SMS and corrected comorbid to epilepsy impaired motor activity, anxiety, memory, and alleviated depressive-like responses measured in the elevated plus maze, object recognition test, radial arm maze test, and sucrose preference test, respectively. This AED suppressed oxidative stress through increased superoxide dismutase activity and glutathione levels, and alleviated catalase activity and lipid peroxidation in the hippocampus. Lacosamide treatment after SE mitigated the increased levels of IL-1β and TNF-α in the hippocampus and exerted strong neuroprotection both in the dorsal and ventral hippocampus, basolateral amygdala, and partially in the piriform cortex. Our results suggest that the antioxidant, anti-inflammatory, and neuroprotective activity of LCM is an important prerequisite for its anticonvulsant and beneficial effects on SE-induced behavioral comorbidities.

scholarly journals Mumijo Traditional Medicine: Fossil Deposits from Antarctica (Chemical Composition and Beneficial Bioactivity)

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Anna Aiello ◽  
Ernesto Fattorusso ◽  
Marialuisa Menna ◽  
Rocco Vitalone ◽  
Heinz C. Schröder ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Traditional Medicine ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Amyloid Peptide ◽  
Neuroprotective Activity ◽  
Antiallergic Activity ◽  
Neuronal Pc12 Cells ◽  
Biomedical Potential

Mumijo is a widely used traditional medicine, especially in Russia, Altai Mountains, Mongolia, Iran Kasachstan and in Kirgistan. Mumijo preparations have been successfully used for the prevention and treatment of infectious diseases; they display immune-stimulating and antiallergic activity as well. In the present study, we investigate the chemical composition and the biomedical potential of a Mumijo(-related) product collected from the Antarctica. The yellow material originates from the snow petrels,Pagodroma nivea. Extensive purification and chemical analysis revealed that the fossil samples are a mixture of glycerol derivatives.In vitroexperiments showed that the Mumijo extract caused in cortical neurons a strong neuroprotective effect against the apoptosis-inducing amyloid peptide fragmentβ-fragment 25–35 (Aβ25–35). In addition, the fraction rich in glycerol ethers/wax esters displayed a significant growth-promoting activity in permanent neuronal PC12 cells. It is concluded that this new Mumijo preparation has distinct and marked neuroprotective activity, very likely due to the content of glycerol ether derivatives.

scholarly journals Neuroprotective Effect of Nevirapine on Cerebral Ischemic Stroke by Middle Cerebral Artery Occlusion in Wistar Rats

2016 ◽  
Vol 1 (01) ◽  
pp. 16-24
Author(s):  
Vasudha Bakshi ◽  
CH Maneesha Ram ◽  
Nazia Begum ◽  
Naveen Pathakala
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Wistar Rats ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Neuroprotective Activity ◽  
Differential Leukocyte Count ◽  
Cognitive Improvement ◽  
Cerebral Artery Occlusion

Objective: To evaluate the neuroprotective effect of Nevirapine on cerebral ischemia stroke by middle cerebral artery occlusion in wistar rats. Methods: The rats were pre and post treated with Nevirapine (NVP) at selective doses (5, 10 mg/kg/g, p.o) for a period of 14 days followed by middle cerebral artery occlusion (MCAO). Neurobehavioral changes were evaluated by using Y-maze and open field habituation. Biochemical markers such as acetyl cholinesterase (AChE), glutamate, differential leukocyte count (DLC), lactate dehydrogenase (LDH), antioxidants such as superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase were estimated. Results: Obtain results revealed that 14 days of treatment with NVP was effective in averting neurotoxicity. NVP treatment significantly reduced AChE, glutamate, DLC, LDH and elevated levels of antioxidant parameters such as SOD, catalase and GPX.. Conclusion: These results clearly revealed that Nevirapine exhibited cognitive improvement which is related to its antioxidant and neuroprotective activity. Further studies are suggested to evaluate molecular mechanism of involved in neuroprotection.

scholarly journals The p75NTR neurotrophin receptor is required to organize the mature neuromuscular synapse by regulating synaptic vesicle availability

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Viviana Pérez ◽  
Francisca Bermedo-Garcia ◽  
Diego Zelada ◽  
Felipe A. Court ◽  
Miguel Ángel Pérez ◽  
...  
Keyword(s):  
Neuromuscular Junction ◽  
Motor Neurons ◽  
Neuromuscular Junctions ◽  
Neuronal Damage ◽  
Neuromuscular Synapse ◽  
Force Production ◽  
Synaptic Function ◽  
Neurotrophin Receptor ◽  
Acetylcholinesterase Inhibition ◽  
Pharmacological Intervention

Abstract The coordinated movement of organisms relies on efficient nerve-muscle communication at the neuromuscular junction. After peripheral nerve injury or neurodegeneration, motor neurons and Schwann cells increase the expression of the p75NTR pan-neurotrophin receptor. Even though p75NTR targeting has emerged as a promising therapeutic strategy to delay peripheral neuronal damage progression, the effects of long-term p75NTR inhibition at the mature neuromuscular junction have not been elucidated. We performed quantitative neuroanathomical analyses of the neuromuscular junction in p75NTR null mice by laser confocal and electron microscopy, which were complemented with electromyography, locomotor tests, and pharmacological intervention studies. Mature neuromuscular synapses of p75NTR null mice show impaired postsynaptic organization and ultrastructural complexity, which correlate with altered synaptic function at the levels of nerve activity-induced muscle responses, muscle fiber structure, force production, and locomotor performance. Our results on primary myotubes and denervated muscles indicate that muscle-derived p75NTR does not play a major role on postsynaptic organization. In turn, motor axon terminals of p75NTR null mice display a strong reduction in the number of synaptic vesicles and active zones. According to the observed pre and postsynaptic defects, pharmacological acetylcholinesterase inhibition rescued nerve-dependent muscle response and force production in p75NTR null mice. Our findings revealing that p75NTR is required to organize mature neuromuscular junctions contribute to a comprehensive view of the possible effects caused by therapeutic attempts to target p75NTR.

scholarly journals Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway

2019 ◽  
Vol 20 (4) ◽  
pp. 998 ◽  
Author(s):  
Yao-Chung Chuang ◽  
Shang-Der Chen ◽  
Chung-Yao Hsu ◽  
Shu-Fang Chen ◽  
Nai-Ching Chen ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Prolonged Seizure

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

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