Passive Movement Improves the Learning and Memory Function of Rats with Cerebral Infarction by Inhibiting Neuron Cell Apoptosis

2013 ◽  
Vol 49 (1) ◽  
pp. 216-221 ◽  
Author(s):  
Man Li ◽  
Jun Peng ◽  
Meng-Die Wang ◽  
Yan-Ling Song ◽  
Yuan-Wu Mei ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Learning And Memory ◽  
Cell Apoptosis ◽  
Memory Function ◽  
Passive Movement

scholarly journals Minocycline improves learning and memory functions in ischemic stroke rats via reduction of cerebral ischemia-induced neuroinflammation and apoptosis

2022 ◽  
Vol 20 (2) ◽  
pp. 287-292
Author(s):  
Li Li ◽  
Xiaolian Xing ◽  
Qian Li ◽  
Qinqin Zhang ◽  
Lu Fu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Protein Expression ◽  
Learning And Memory ◽  
Cell Apoptosis ◽  
Expression Level ◽  
Control Group ◽  
Volume Number ◽  
Memory Functions

Purpose: To study the effect minocycline on learning and memory functions in ischemic stroke rats, and the underlying mechanism. Methods: 60 adult male SD rats were randomly divided into control group, ischemic brain damage (6 and 24 h MACO) groups; and 6 and 24 h minocycline groups, with 12 rats in each group. The volume of cerebral infarction, neuronal cell apoptosis, NF-κB protein expression, learning and memory ability, and the number of Iba-1+CD206-positive cells, and CD206/CD68 mRNA expressions in sham group, 6 h MACO group and 6 h minocycline group were determined and compared. Results: The number of iba-1 +CD206-positive cells, expression level of CD206 mRNA, frequency of platform crossing, and percentage of third quadrant route in 6 h minocycline group were significantly higher than the corresponding values in 6 h MACO group. However, the cerebral infarction volume, number of Nini-positive cells, and the NF- B protein expression levels were markedly reduced, relative to corresponding values in 6 h MACO rats. The number of iba-1+CD206-positive cells was significantly lower in 6 h MACO rats than in sham rats, while the expression level of CD68 mRNA was significantly higher (p < 0.05). The number of TUNEL-positive cells in 6 and 24 h minocycline groups were markedly lower than that in 6 h MACO group (p < 0.05). Conclusion: Minocycline improves learning and memory of ischemic stroke rats by relieving the neuroinflammation induced by cerebral ischemia and cell apoptosis. Thus, the compound can be further developed for management learning and memory deficits in stroke patients.

Continuous VA deficiency during postnatal development decreases rat learning and memory function via excitatory Ca2+neuron

2010 ◽  
Vol 34 (8) ◽  
pp. S18-S18
Author(s):  
Wei Jiang ◽  
Enyi Wen ◽  
Min Gong ◽  
Yang Bi ◽  
Xiaojuan Zhang ◽  
...  
Keyword(s):  
Postnatal Development ◽  
Learning And Memory ◽  
Memory Function

scholarly journals Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

2015 ◽  
Vol 35 (9) ◽  
pp. 1435-1444 ◽  
Author(s):  
Tingting Dong ◽  
Qi Zhang ◽  
Michael R Hamblin ◽  
Mei X Wu
Keyword(s):  
Learning And Memory ◽  
Memory Function ◽  
Light Illumination ◽  
Low Level ◽  
Metabolic Substrates ◽  
Secondary Damage ◽  
Injured Brain ◽  
Combinational Treatment

Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue–like injured brain.

Effects of Gossypium herbaceam Extract Administration on the Learning and Memory Function in the Naturally Aged Rats: Neuronal Niche Improvement1

2012 ◽  
Vol 31 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Yanyong Liu ◽  
Haji Akber Aisa ◽  
Chao Ji ◽  
Nan Yang ◽  
Haibo Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Aged Rats

Aging-associated cognitive impairment is an important health care issue since individuals with mild cognitive impairment are more likely to develop Alzheimer’s disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment associated with aging were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70, and 140 mg/kg exerted an improved effect on the learning and memory impairment in aged rats. Subsequently, GHE afforded a beneficial action on eradication of free radicals without influence on the activity of glutathione peroxidase and superoxide dismutase. GHE treatment enhanced the expression levels of nerve growth factor. Meanwhile, proliferation of neural progenitor cells was elevated in hippocampus after treatment with GHE. Taken together, neurogenic niche improvement could be involved in the mechanism underlying neuroprotection of GHE against aging-associated cognitive impairment. These findings suggested that GHE might be a potential agent as cognitive-enhancing drugs that delay or halt mild cognitive impairment progression to Alzheimer’s disease or treatment of aging-associated cognitive impairment.

scholarly journals Effects of Malania oleifera Chun Oil on the Improvement of Learning and Memory Function in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Rui Wu ◽  
Shaoqi Zhong ◽  
Mengmei Ni ◽  
Xuejiao Zhu ◽  
Yiyi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Memory Function ◽  
Nervonic Acid ◽  
Acetyl Cholinesterase ◽  
Behavioral Experiments ◽  
Memory Impairments ◽  
Oxidative Stress Parameters ◽  
Algae Oil ◽  
Different Doses

Background. The fruits of Malania oleifera Chun & S. K. Lee have been highly sought after medically because its seeds have high oil content (>60%), especially the highest known proportion of nervonic acid (>55%). Objective of the Study. The objective was to explore the effects of different doses of Malania oleifera Chun oil (MOC oil) on the learning and memory of mice and to evaluate whether additional DHA algae oil and vitamin E could help MOC oil improve learning and memory and its possible mechanisms. Methods. After 30 days of oral administration of the relevant agents to mice, behavioral tests were conducted as well as detection of oxidative stress parameters (superoxide dismutase, malondialdehyde, and glutathione peroxidase) and biochemical indicators (acetylcholine, acetyl cholinesterase, and choline acetyltransferase) in the hippocampus. Results. Experimental results demonstrated that MOC oil treatment could markedly improve learning and memory of mouse models in behavioral experiments and increase the activity of GSH-PX in hippocampus and reduce the content of MDA, especially the dose of 46.27 mg/kg. The addition of DHA and VE could better assist MOC oil to improve the learning and memory, and its mechanism may be related to the inhibition of oxidative stress and restrain the activity of AChE and also increase the content of ACh. Conclusion. Our results demonstrated that MOC oil treatment could improve learning and memory impairments. Therefore, we suggest that MOC oil is a potentially important resource for the development of nervonic acid products.

scholarly journals Human Umbilical Cord-Derived Mesenchymal Stem Cells Improve Learning and Memory Function in Hypoxic-Ischemic Brain-Damaged Rats via an IL-8-Mediated Secretion Mechanism Rather than Differentiation Pattern Induction

2015 ◽  
Vol 35 (6) ◽  
pp. 2383-2401 ◽  
Author(s):  
Xiaoqin Zhou ◽  
Jialu Gu ◽  
Yan Gu ◽  
Mulan He ◽  
Yang Bi ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Umbilical Cord ◽  
Memory Function ◽  
Morphological Characteristics ◽  
Human Umbilical Cord ◽  
Therapeutic Effects ◽  
Differentiation Potential ◽  
Ischemic Brain ◽  
Differentiation Pattern

Background: MSCs are a promising therapeutic resource. Paracrine effects and the induction of differentiation patterns are thought to represent the two primary mechanisms underlying the therapeutic effects of mesenchymal stem cell (MSC) transplantation in vivo. However, it is unclear which mechanism is involved in the therapeutic effects of human umbilical cord-derived MSC (hUC-MSC) transplantation. Methods and Results: Based on flow cytometry analysis, hUC-MSCs exhibited the morphological characteristics and surface markers of MSCs. Following directed neural induction, these cells displayed a neuron-like morphology and expressed high levels of neural markers. All types of hUC-MSCs, including differentiated and redifferentiated cells, promoted learning and memory function recovery in hypoxic-ischemic brain damaged (HIBD) rats. The hUC-MSCs secreted IL-8, which enhanced angiogenesis in the hippocampus via the JNK pathway. However, the differentiated and redifferentiated cells did not exert significantly greater therapeutic effects than the undifferentiated hUC-MSCs. Conclusion: hUC-MSCs display the biological properties and neural differentiation potential of MSCs and provide therapeutic advantages by secreting IL-8, which participates in angiogenesis in the rat HIBD model. These data suggest that hUC-MSC transplantation improves the recovery of neuronal function via an IL-8-mediated secretion mechanism, whereas differentiation pattern induction was limited.

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