scholarly journals Cholinergic Enhancing and Antioxidant Effect of Vigna subterranea (L.) Verdc. (Fabaceae) Landrace Aqueous Extract on Scopolamine-Induced Amnesia in Male Swiss Mice

2020 ◽  
Vol 70 (12) ◽  
pp. 4336-4347
Author(s):  
Herve Herve Ngatanko Abaissou ◽  
Foyet Harquin Simplice ◽  
Eglantine Keugong Wado ◽  
Balbine Kamleu Nkwingwa ◽  
Jorelle Linda Damo Kamda ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Aqueous Extract ◽  
Memory Impairment ◽  
Escape Latency ◽  
Cell Damage ◽  
Protective Action ◽  
Acetylcholine Esterase ◽  
Protective Effects ◽  
Vigna Subterranea ◽  
Y Maze

The present study was conducted to investigate protective effects of the aqueous extract of V. subterranea seeds landrace on amnesia induced by scopolamine in mice. V. subterranea aqueous extract (100, 200 and 400 mg/kg BW) was administered by gavage for nine consecutive days and memory impairment was induced by repeated intraperitoneal injection of scopolamine (1.5 mg/kg). The Y-maze (YM), Morris water maze (MWM), novel object recognition paradigm (NOR) and the T maze (TM) were used to assess learning, memory and retention. Superoxide dismutase (SOD), Catalase (CAT), Malondialdehyde (MDA) levels and Acetylcholine esterase activity was also evaluated in the mice hippocampi homogenates. V. subterranea aqueous extract (400 mg/kg) significantly increased the percentage of spontaneous alternation in the YM task and decreased escape latency in the MWM. Moreover, this dose brought about a significantly improvement in the time spent in the preferred TM arm and discrimination index in the NOR tasks despite repeated scopolamine injection. Additionally, low acetylcholine esterase levels, reduced lipid peroxidation (malondialdehyde) but increased antioxidant enzymes (catalase and superoxide dismutase) activity was observed in hippocampi homogenate of mice pre-treated with the extract. A protective action against hippocampal cell damage was also evident. This finding suggests that the aqueous extract of V. subterranea seed landrace may improve learning and memory.

scholarly journals Ziziphus jujuba (Rhamnaceae) Alleviates Working Memory Impairment and Restores Neurochemical Alterations in the Prefrontal Cortex of D-Galactose-Treated Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Antoine K. Kandeda ◽  
Danide Nguedia ◽  
Espoir R. Ayissi ◽  
Jonas Kouamouo ◽  
Théophile Dimo
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Aqueous Extract ◽  
Spontaneous Alternation ◽  
Memory Impairment ◽  
Distilled Water ◽  
The Novel ◽  
Novel Object ◽  
Y Maze ◽  
Ziziphus Jujuba

Alzheimer’s disease is a progressive cognitive dysfunction. However, pharmacological treatments are symptomatic and have many side effects, opening the opportunity to alternative medicine. This study investigated the antiamnesic effect of the aqueous extract of Ziziphus jujuba on D-galactose-induced working memory impairment in rats. Impairment of working memory was induced by subcutaneous (s.c.) injection of D-galactose (350 mg/kg/day) to rats for 21 days. These animals were then subjected to object recognition and Y-maze tests. Rats with confirmed memory impairment were treated per os (p.o.) with tacrine (10 mg/kg), aspirin (20 mg/kg, p.o.), extract (41.5, 83, and 166 mg/kg, p.o.), and distilled water (10 mL/kg, p.o.) daily for 14 days. At the end of the treatments, alteration in working memory was assessed using the above paradigms. Afterward, these animals were euthanized, and cholinergic, proinflammatory, and neuronal damage markers were analyzed in the prefrontal cortex. Rats administered D-galactose and treated with distilled water had impaired working memory (evidenced by decreased time spent on the novel object and discrimination index) and decreased spontaneous alternation in the Y-maze. D-galactose also decreased the levels of acetylcholinesterase and acetylcholine and increased the level of glial fibrillary acidic protein, ionized calcium-binding adapter molecule 1, tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and interferon-gamma (IFN-γ). Treatment with the extract (166 mg/kg) reversed the time spent on the novel object and the discrimination index. It equally increased the percentage of spontaneous alternation. Neurochemical analysis revealed that the extract markedly alleviated acetylcholinesterase activity and neuroinflammation. These observations were corroborated by the reduction in neuronal loss. Taken together, these results suggest that Ziziphus jujuba aqueous extract possesses an antiamnesic effect. This effect seems to involve cholinergic and anti-inflammatory modulations. This, therefore, claims using this plant in the treatment of dementia in Cameroon subject to further studies and trials.

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

2021 ◽  
pp. 096032712110099
Author(s):  
H Liu ◽  
M Wang ◽  
L Xu ◽  
M Li ◽  
M Zhao
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Target Genes ◽  
Escape Latency ◽  
Neuroprotective Effect ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spatial Learning And Memory ◽  
Protective Effects ◽  
Factor Α

Background: Isoflurane, one of the most commonly used inhalational anesthetics, is usually used in surgery patients and often causes long-term learning and memory impairment. The aim of this study was to explore the role of microRNA-204-5p (miR-204-5p) in isoflurane-induced learning and memory impairment in rats. Methods: The Morris Water Maze (MWM) test was used to estimate the spatial learning and memory abilities of laboratory rats. Enzyme-linked immunosorbent assay (ELISA) was used to determine interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) concentrations in the hippocampal tissues. The expression level of miR-204-5p was determined by using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The potential target genes of miR-204-5p were predicted and verified by the TargetScan and dual-luciferase reporter assay, respectively. Results: Isoflurane-induced rats showed significantly higher neurological function scores, higher escape latency and shorter time spent in the original quadrant. Isoflurane could significantly induce neuroinflammation, and the expression of miR-204-5p was increased in the hippocampal tissue of rats exposed to isoflurane. Moreover, downregulation of miR-204-5p attenuated the effect of isoflurane treatment on the escape latency and the time in the original quadrant, and inflammatory cytokines level was downregulated by inhibiting the expression of miR-204-5p. EphB2 was verified as a direct target gene of miR-204-5p. Conclusion: Downregulated miR-204-5p exerts protective effects against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation. MiR-204-5p could serve as a potential therapeutic target for the lightening of cognitive dysfunction induced by isoflurane.

scholarly journals Synergistic Effect of Quercetin and α-Lipoic Acid on Aluminium Chloride Induced Neurotoxicity in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Sooad Saud Al-Otaibi ◽  
Maha Mohamad Arafah ◽  
Bechan Sharma ◽  
Abdullah Salih Alhomida ◽  
Nikhat Jamal Siddiqi
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Body Weight ◽  
Glutathione Reductase ◽  
Lipoic Acid ◽  
Reduced Glutathione ◽  
Protein Carbonyl ◽  
Acetylcholine Esterase ◽  
Aluminium Chloride ◽  
Protective Effects

Objectives. The present study was carried out to study the protective effects of quercetin and α-lipoic acid alone and in combination against aluminum chloride induced neurotoxicity in rats. Materials and Methods. The study consisted of eight groups, namely, Group 1: control rats, Group 2: rats receiving aluminium chloride 7 mg/kg body weight intraperitoneal route (i.p) for two weeks, Group 3: rats receiving quercetin 50 mg/kg body weight i.p. for two weeks, Group 4: rats receiving quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 5: rats receiving α-lipoic acid 20 mg/kg body weight i.p. for two weeks, Group 6: rats receiving lipoic acid 20 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks, Group 7: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight i.p. for two weeks, and Group 8: rats receiving α-lipoic acid 20 mg/kg body weight and quercetin 50 mg/kg body weight followed by aluminium chloride 7 mg/kg body weight i.p. for two weeks. The animals were killed after 24 hours of the last dose by cervical dislocation. Results. Aluminium chloride treatment of rats resulted in significant increases in lipid peroxidation, protein carbonyl levels, and acetylcholine esterase activity in the brain. This was accompanied with significant decreases in reduced glutathione, activities of the glutathione reductase, and superoxide dismutase. Pretreatment of AlCl3 exposed rats to either quercetin or α-lipoic acid also restored altered lipid peroxidation and superoxide dismutase to near normal levels. Quercetin or α-lipoic acid pretreatment of AlCl3 exposed rats improved the protein carbonyl and reduced glutathione, glutathione reductase, and acetylcholine esterase activities in rat brains towards normal levels. Combined pretreatment of AlCl3 exposed rats with quercetin and α-lipoic acid resulted in a tendency towards normalization of most of the parameters. Conclusions. Quercetin and α-lipoic acid complemented each other in protecting the rat brain against oxidative stress induced by aluminium chloride.

scholarly journals Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

2015 ◽  
Vol 37 (2) ◽  
pp. 465-476 ◽  
Author(s):  
Xin-Tao Wang ◽  
Ye Tian ◽  
Wen-Xiao Xu ◽  
Li-Huang Cui ◽  
Shou-Yang Xiang ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Coordination Compound ◽  
Skeletal Muscles ◽  
Structural Changes ◽  
Ischemia Reperfusion Injury ◽  
Morphological Changes ◽  
Ischemia Reperfusion ◽  
Protective Action ◽  
Critical Role ◽  
Protective Effects

Background/Aim: Ischemia/reperfusion (I/R) injury of skeletal muscles is common pathophysiology during surgeries and the superoxide dismutase (SOD) plays a critical role in this process. SOD-modeled coordination compound (MSODa) may simulate the protective effects as SOD. Methods: Therefore, this study was designed to explore the protective effects and underlying mechanism of MSODa on malondialdehyde (MDA) and integrin-β2 (CD11b/CD18) in plasma, myeloperoxidase (MPO) and intercellular cell adhesion molecule-1 (ICAM-1) in tissue, and morphological changes before and after I/R injury. The rat model of I/R in hind limb was established and randomly divided into sham, ischemia, I/R, I/R-treated with saline, SOD, and MSODa, respectively. Results: These results showed that averaged values for MDA, MPO, CD11b/CD18, and ICAM-1 were significantly increased (P < 0.01 vs ischemia alone) in a time-dependent fashion along with marked tissue remodeling, such as abnormal arrangement of muscular fibers, interstitial edema, vasodilation with no-reflow, inflammatory cells adherent and infiltration, structural changes in mitochondrial, and decrease in glycogens as well. However, all parameter changes induced by I/R injury were reversed, at least partially, by MSODa and SOD treatments and intriguingly, the beneficial/protective effects of MSODa was superior to SOD with an early onset. Conclusion: This novel finding demonstrates that MSODa improves I/R injury of skeletal muscles due at least partially to inhibition of adherent molecule expression and reduction of oxygen free radical formation during I/R pathophysiological processes and this protective action of MSODa was superior to SOD, highlighting the bright future for MSODa in clinical management of tissue I/R injury.

The Protective Action of the Aqueous Extract of Auricularia polytricha in Paracetamol Induced Hepatotoxicity in Rats

2016 ◽  
Vol 10 (1) ◽  
pp. 72-76 ◽  
Author(s):  
Dinesh K. Chellappan ◽  
Sivamalar Ganasen ◽  
Shaminiswary Batumalai ◽  
Mayuren Candasamy ◽  
Purushotham Krishnappa ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Protective Action ◽  
Auricularia Polytricha

scholarly journals Combined Effects of Carotenoids and Polyphenols in Balancing the Response of Skin Cells to UV Irradiation

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1931
Author(s):  
Glenda Calniquer ◽  
Marina Khanin ◽  
Hilla Ovadia ◽  
Karin Linnewiel-Hermoni ◽  
David Stepensky ◽  
...  
Keyword(s):  
Cell Damage ◽  
Plasma Concentrations ◽  
Dermal Fibroblasts ◽  
Carnosic Acid ◽  
Rosemary Extract ◽  
Protective Effects ◽  
Skin Cells ◽  
Tomato Extract ◽  
Clinical Experiments

Oral carotenoids and polyphenols have been suggested to induce photo-protective effects. The aim of the study was to test whether the combination of carotenoids and polyphenols produce greater protective effects from UV-induced damage to skin cells. Such damage is characterized by inflammation and oxidative stress; thus, the photo-protective effect can be partially explained by modulating the nuclear factor kappa B (NFκB) and antioxidant response element/Nrf2 (ARE/Nrf2) transcription systems, known as important regulators of these two processes. Indeed, it was found in keratinocytes that carotenoids and polyphenols inhibit UVB-induced NFκB activity and release of cytokine IL-6. A combination of tomato extract with rosemary extract inhibited UVB-induced release of IL-6 more than each of the compounds alone. Moreover, this combination synergistically activated ARE/Nrf2 transcription systems. Inflammatory cytokines such as IL-6 and TNFα induce the expression of matrix metalloproteinases (MMPs), which leads to collagen breakdown; thus, it is important to note that carnosic acid reduced TNFα-induced MMP-1 secretion from human dermal fibroblasts. The in vitro results suggest beneficial effects of phytonutrient combinations on skin health. To assure that clinical experiments to prove such effects in humans are feasible, the human bioavailability of carotenoids from tomato extract was tested, and nearly a twofold increase in their plasma concentrations was detected. This study demonstrates that carotenoids and polyphenols cooperate in balancing UV-induced skin cell damage, and suggests that NFκB and ARE/Nrf2 are involved in these effects.

scholarly journals Norepinephrine Protects against Methamphetamine Toxicity through β2-Adrenergic Receptors Promoting LC3 Compartmentalization

2021 ◽  
Vol 22 (13) ◽  
pp. 7232
Author(s):  
Gloria Lazzeri ◽  
Carla L. Busceti ◽  
Francesca Biagioni ◽  
Cinzia Fabrizi ◽  
Gabriele Morucci ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Light Chain ◽  
Adrenergic Receptors ◽  
Cell Damage ◽  
Protective Effects ◽  
Autophagy Flux ◽  
Brain Areas ◽  
Indirect Consequence

Norepinephrine (NE) neurons and extracellular NE exert some protective effects against a variety of insults, including methamphetamine (Meth)-induced cell damage. The intimate mechanism of protection remains difficult to be analyzed in vivo. In fact, this may occur directly on target neurons or as the indirect consequence of NE-induced alterations in the activity of trans-synaptic loops. Therefore, to elude neuronal networks, which may contribute to these effects in vivo, the present study investigates whether NE still protects when directly applied to Meth-treated PC12 cells. Meth was selected based on its detrimental effects along various specific brain areas. The study shows that NE directly protects in vitro against Meth-induced cell damage. The present study indicates that such an effect fully depends on the activation of plasma membrane β2-adrenergic receptors (ARs). Evidence indicates that β2-ARs activation restores autophagy, which is impaired by Meth administration. This occurs via restoration of the autophagy flux and, as assessed by ultrastructural morphometry, by preventing the dissipation of microtubule-associated protein 1 light chain 3 (LC3) from autophagy vacuoles to the cytosol, which is produced instead during Meth toxicity. These findings may have an impact in a variety of degenerative conditions characterized by NE deficiency along with autophagy impairment.

scholarly journals Isorhynchophylline Protects PC12 Cells Against Beta-Amyloid-Induced Apoptosis via PI3K/Akt Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yan-Fang Xian ◽  
Zhi-Xiu Lin ◽  
Qing-Qiu Mao ◽  
Jian-Nan Chen ◽  
Zi-Ren Su ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Glycogen Synthase ◽  
Neuroprotective Effect ◽  
Protective Action ◽  
Protective Effects ◽  
Phosphorylated Akt ◽  
Induced Apoptosis

The neurotoxicity of amyloid-β(Aβ) has been implicated as a critical cause of Alzheimer’s disease. Isorhynchophylline (IRN), an oxindole alkaloid isolated fromUncaria rhynchophylla,exerts neuroprotective effect againstAβ25–35-induced neurotoxicityin vitro. However, the exact mechanism for its neuroprotective effect is not well understood. The present study aimed to investigate the molecular mechanisms underlying the protective action of IRN againstAβ25–35-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Pretreatment with IRN significantly increased the cell viability, inhibited the release of lactate dehydrogenase and the extent of DNA fragmentation inAβ25–35-treated cells. IRN treatment was able to enhance the protein levels of phosphorylated Akt (p-Akt) and glycogen synthase kinase-3β(p-GSK-3β). Lithium chloride blockedAβ25–35-induced cellular apoptosis in a similar manner as IRN, suggesting that GSK-3βinhibition was involved in neuroprotective action of IRN. Pretreatment with LY294002 completely abolished the protective effects of IRN. Furthermore, IRN reversedAβ25–35-induced attenuation in the level of phosphorylated cyclic AMP response element binding protein (p-CREB) and the effect of IRN could be blocked by the PI3K inhibitor. These experimental findings unambiguously suggested that the protective effect of IRN againstAβ25–35-induced apoptosis in PC12 cells was associated with the enhancement of p-CREB expression via PI3K/Akt/GSK-3βsignaling pathway.

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