scholarly journals Propolis increases neuronal count in hippocampal area CA1 and prefrontal cortex in stressed rats

2017 ◽  
Vol 36 (3) ◽  
pp. 214
Author(s):  
Kuswati Nugroho ◽  
Ety Sari Handayani ◽  
Zainuri Sabta Nugraha
Keyword(s):  
Prefrontal Cortex ◽  
Cell Count ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Sprague Dawley ◽  
Stress Group ◽  
Induced Stress ◽  
Area Ca1 ◽  
Sprague Dawley Rats ◽  
Hippocampal Area

Background <br />Stress induces neuronal cell damage in the hippocampus and prefrontal cortex. Propolis has a neuroprotective effect that can inhibit apoptosis and decrease neuronal cell count. This study aimed to determine the effect of propolis on neuronal cell count in hippocampal area CA1 and prefrontal cortex in Sprague Dawley rats with induced stress.<br /><br />Methods<br />A study of laboratory experimental design was conducted involving 24 male Sprague-Dawley Rattus norvegicus. The animals were randomly divided into 4 groups, i.e. controls (K), and stress groups P1, P2 and P3. Controls did not receive treatment, stress group (P1) received stress treatment, groups P2 and P3 received stress and propolis at 100 and 200 mg/kgBW, respectively. Stress and propolis were given for 14 days, followed by termination. The number of neurons in the hippocampal area CA1 and prefrontal cortex were counted. One way ANOVA was used to analyze the data.<br /><br />Results <br />The neuronal count in the hippocampal area CA1 and prefrontal cortex in the stress group (P1) was lower than in groups K, P2 and P3. There were significant differences in the neuronal count of the hippocampal area CA1 between P1 and P3 and P1 and K (p=0.019) and also in the neuronal count of the prefrontal cortex between P1 and P2, P3 and K (p=0.002).<br /><br />Conclusions <br />This study strongly suggest that propolis inhibits the decrease in neuronal count in in the hippocampal area CA1 and prefrontal cortex of Sprague Dawley rats with induced stress. The present study suggests a potential neuroprotective effect of propolis in the prevention of neurodegenerative disorders.

scholarly journals Neuroprotective Effect of Gui Zhi (Ramulus Cinnamomi) on Ma Huang- (Herb Ephedra-) Induced Toxicity in Rats Treated with a Ma Huang-Gui Zhi Herb Pair

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Fang-hao Zheng ◽  
Ping Wei ◽  
Hui-ling Huo ◽  
Xue-feng Xing ◽  
Fei-long Chen ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Oxidative Damage ◽  
Neuroprotective Effect ◽  
Inhibitory Effect ◽  
Chinese Herbs ◽  
Clinical Use ◽  
Sprague Dawley ◽  
Neuroprotective Effects ◽  
Sprague Dawley Rats ◽  
Ma Huang

Herb Ephedra(Ma Huang in Chinese) andRamulus Cinnamomi(Gui Zhi in Chinese) are traditional Chinese herbs, often used together to treat asthma, nose and lung congestion, and fever with anhidrosis. Due to the adverse effects of ephedrine, clinical use of Ma Huang is restricted. However, Gui Zhi extract has been reported to decrease spontaneous activity in rats and exert anti-inflammatory and neuroprotective effects. The present study explored the possible inhibitory effect of Gui Zhi on Ma Huang-induced neurotoxicity in rats when the two herbs were used in combination. All Ma Huang and Ma Huang-Gui Zhi herb pair extracts were prepared using methods of traditional Chinese medicine and were normalized based on the ephedrine content. Two-month-old male Sprague-Dawley rats (n=6rats/group) were administered Ma Huang or the Ma Huang-Gui Zhi herb pair extracts for 7 days (ephedrine = 48 mg/kg), and locomotor activity was measured. After 7 days, oxidative damage in the prefrontal cortex was measured. Gui Zhi decreased hyperactivity and sensitization produced by repeated Ma Huang administration and attenuated oxidative stress induced by Ma Huang. The results of this study demonstrate the neuroprotective potential of Gui Zhi in Ma Huang-induced hyperactivity and oxidative damage in the prefrontal cortex of rats when used in combination.

scholarly journals Centella asiatica increases B-cell lymphoma 2 expression in rat prefrontal cortex

2016 ◽  
Vol 34 (1) ◽  
pp. 10
Author(s):  
Kuswati Kuswati ◽  
Djoko Prakosa ◽  
Brian Wasita ◽  
Nanang Wiyono
Keyword(s):  
Prefrontal Cortex ◽  
B Cell ◽  
Restraint Stress ◽  
Centella Asiatica ◽  
Ethanol Extract ◽  
B Cell Lymphoma ◽  
Control Group ◽  
Sprague Dawley ◽  
Stress Group ◽  
Sprague Dawley Rats

<p>BACKGROUND<br />Stress is one of the factors that cause apoptosis in neuronal cells. Centella<br />asiatica has a neuroprotective effect that can inhibit apoptosis. This study<br />aimed to examine the effect of Centella asiatica ethanol extract on B-cell<br />lymphoma 2 (Bcl-2) protein expression in the prefrontal cortex of rats.</p><p>METHODS<br />An experimental study was conducted on 34 brain tissue samples from male<br />Sprague Dawley rats exposed to chronic restraint stress for 21 days. The<br />samples were taken from following groups: non-stress group K, negative<br />control group P1 (stress + arabic gum powder), P2 (stress + C.asiatica at<br />150 mg/kgBW), P3 (stress + C.asiatica at 300 mg/kg BW), P4 (stress +<br />C.asiatica at 600 mg/kg body weight) and positive control group P5 (stress<br />+ fluoxetine at 10 mg/kgBW). The samples were made into sections that<br />were stained immunohistochemically using Bcl-2 antibody to determine the<br />percentage of cells expressing Bcl-2. Data were analyzed using one way<br />ANOVA test followed by a post - hoc test.</p><p>RESULTS<br />There were significant differences in mean Bcl-2 expression between the<br />groups receiving Centella asiatica compared with the non-stress group and<br />stress-only group (negative control group) (p&lt;0.05). The results were<br />comparable to those of the fluoxetine treatment group.</p><p>CONCLUSION</p><p>The Centella asiatica ethanol extract was able to increase Bcl-2 expression<br />in the prefrontal cortex of Sprague Dawley rats exposed to restraint stress.<br />This study suggests that Centella asiatica may be useful in the treatment of<br />cerebral stress.</p>

Curcumin Reduces Neuroinflammation and Improves the Impairments of Anesthetics on Learning and Memory by Regulating the Expression of miR-181a-5p

2021 ◽  
pp. 1-9
Author(s):  
Guizhen Liu ◽  
Yuchuan Sun ◽  
Fei Liu
Keyword(s):  
Cognitive Impairment ◽  
Protective Effect ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Inflammatory Cytokines ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Sprague Dawley Rats

<b><i>Objective:</i></b> The purpose of this study was to explore the role of curcumin (Cur) in isoflurane (ISO)-induced learning and memory dysfunction in Sprague-Dawley rats and further elucidate the mechanism of the protective effect produced by Cur. <b><i>Methods:</i></b> Rat models of cognitive impairment were established by inhaling 3% ISO. The Morris water maze test was used to assess the cognitive function of rats. ELISA and qRT-PCR were used to analyze the protein levels of pro-inflammatory cytokines and expression levels of miR-181a-5p, respectively. <b><i>Results:</i></b> Cur significantly improved the ISO-induced cognitive dysfunction in rats and alleviated the ISO-induced neuroinflammation. miR-181a-5p was overexpressed in ISO-induced rats, while Cur treatment significantly reduced the expression of miR-181a-5p. Overexpression of miR-181a-5p promoted the cognitive impairment and the release of inflammatory cytokines and reversed the neuroprotective effect of Cur. <b><i>Conclusion:</i></b> Cur has a protective effect on ISO-induced cognitive dysfunction, which may be achieved by regulating the expression of miR-181a-5p.

Rearrangement of the dendritic morphology of the neurons from prefrontal cortex and hippocampus after subthalamic lesion in Sprague-Dawley rats

Synapse ◽  
2013 ◽  
Vol 68 (3) ◽  
pp. 114-126 ◽  
Author(s):  
Israel Camacho-Abrego ◽  
Gullermina Tellez-Merlo ◽  
Angel I. Melo ◽  
Antonio Rodríguez-Moreno ◽  
Linda Garcés ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Dendritic Morphology ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Augmenting saturated LTP by broadly spaced episodes of theta-burst stimulation in hippocampal area CA1 of adult rats and mice

2014 ◽  
Vol 112 (8) ◽  
pp. 1916-1924 ◽  
Author(s):  
Guan Cao ◽  
Kristen M. Harris
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Sprague Dawley ◽  
Theta Burst Stimulation ◽  
Burst Stimulation ◽  
Cellular Mechanisms ◽  
Adult Rats ◽  
Area Ca1 ◽  
Hippocampal Area ◽  
Theta Burst

Hippocampal long-term potentiation (LTP) is a model system for studying cellular mechanisms of learning and memory. Recent interest in mechanisms underlying the advantage of spaced over massed learning has prompted investigation into the effects of distributed episodes of LTP induction. The amount of LTP induced in hippocampal area CA1 by one train (1T) of theta-burst stimulation (TBS) in young Sprague-Dawley rats was further enhanced by additional bouts of 1T given at 1-h intervals. However, in young Long-Evans (LE) rats, 1T did not initially saturate LTP. Instead, a stronger LTP induction paradigm using eight trains of TBS (8T) induced saturated LTP in hippocampal slices from both young and adult LE rats as well as adult mice. The saturated LTP induced by 8T could be augmented by another episode of 8T following an interval of at least 90 min. The success rate across animals and slices in augmenting LTP by an additional episode of 8T increased significantly with longer intervals between the first and last episodes, ranging from 0% at 30- and 60-min intervals to 13–66% at 90- to 180-min intervals to 90–100% at 240-min intervals. Augmentation above initially saturated LTP was blocked by the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovaleric acid (d-APV). These findings suggest that the strength of induction and interval between episodes of TBS, as well as the strain and age of the animal, are important components in the augmentation of LTP.

Chronic agomelatine administration modulates neuronal plasticity markers in the rat prefrontal cortex, hippocampus and amygdala

2011 ◽  
Vol 26 (S2) ◽  
pp. 652-652
Author(s):  
N. Ladurelle ◽  
C. Potard ◽  
C. Gabriel-Gracia ◽  
E. Mocaër ◽  
E. Beaulieu ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Neuronal Plasticity ◽  
Microtubule Dynamics ◽  
Rat Hippocampus ◽  
Stable Form ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Cytoskeletal Dynamics ◽  
Synaptic Markers

Neuronal plasticity alterations including cytoskeletal dynamics and synaptic markers have been recently associated with the treatment of major depression. Here we investigated the effects of agomelatine, a novel antidepressant with melatonergic (MT1/MT2) agonist and 5-HT2C receptor antagonist properties, on cytoskeletal microtubular proteins and synaptic markers in the rat hippocampus, prefrontal cortex (PFC) and amygdala.Adult male Sprague Dawley rats received daily i.p. administration of hydroxyethylcellulose 1% (vehicle) or agomelatine (40mg/kg) for 22 days. The rats were then sacrificed and hippocampi, PFC and amygdala dissected for analyses of microtubule dynamics markers (Tyr/Glu-Tub, Delta2-Tub and Acet-Tub) and synaptic markers (synaptophysin, PSD-95 and spinophilin) by Western blot.In the PFC, agomelatine decreased Tyr/Glu-Tub and the neuronal-specific Delta2-Tub, suggesting decreased microtubule dynamics. In contrast, in the hippocampus Tyr/Glu-Tub and Delta2-Tub were increased, indicative of enhanced microtubule dynamics. A similar pattern to those seen in the hippocampus, but of higher magnitude, was observed in the amygdala where an important increase of Tyr/Glu-Tub accompanied by a decrease of the stable form Acet-Tub was observed. These findings were paralleled by decreased hippocampal spinophilin (dendritic spines marker), increased synaptophysin (pre-synaptic marker) and spinophilin in the PFC and amygdala and increased PSD-95 (post-synaptic marker) in the amygdala, all consistent with synaptic remodelling phenomena.Taken together, these data shown that chronic agomelatine induces a differential modulation of microtubule dynamics and synaptic markers in the rat hippocampus, PFC and amygdala. These findings may have a particular relevance considering the fundamental role of these three brain areas in depression.

scholarly journals Effect of Ranirestat, a New Aldose Reductase Inhibitor, on Diabetic Retinopathy in SDT Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Fumihiko Toyoda ◽  
Yoshiaki Tanaka ◽  
Ayumi Ota ◽  
Machiko Shimmura ◽  
Nozomi Kinoshita ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Aldose Reductase ◽  
Reductase Inhibitor ◽  
Retinal Thickness ◽  
Neuroprotective Effect ◽  
Treated Group ◽  
Aldose Reductase Inhibitor ◽  
Untreated Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Purpose. To evaluate the effect of ranirestat, a new aldose reductase inhibitor (ARI), on diabetic retinopathy (DR) in Spontaneously Diabetic Torii (SDT) rats.Methods. The animals were divided into six groups, normal Sprague-Dawley rats(n=8), untreated SDT rats(n=9), ranirestat-treated SDT rats (0.1, 1.0, and 10 mg/kg/day,n=7, 8, and 6, resp.), and epalrestat-treated SDT rats (100 mg/kg/day,n=7). Treated rats received oral ranirestat or epalrestat once daily for 40 weeks after the onset of diabetes. After the eyes were enucleated, the retinal thickness and the area of stained glial fibrillary acidic protein (GFAP) were measured.Results. The retinas in the untreated group were significantly thicker than those in the normal and ranirestat-treated (0.1, 1.0, and 10 mg/kg/day) groups. The immunostained area of GFAP in the untreated group was significantly larger than that in the normal and ranirestat-treated (1.0 and 10 mg/kg/day) groups. There were no significant differences between the untreated group and epalrestat-treated group in the retinal thickness and the area of stained GFAP.Conclusion. Ranirestat reduced the retinal thickness and the area of stained GFAP in SDT rats and might suppress DR and have a neuroprotective effect on diabetic retinas.

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