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Background: Depression is the most common psychiatric disorder affecting around 5% of the population worldwide. It leads to morbidity and affects quality of life. Monosodium glutamate (MSG) popularly called a tastemaker is used as a food additive in fast food and other processed foods. MSG has been implicated in causing depression. Since many adolescents and children are being habituated to fast foods, the current study is to evaluate the effects of polyunsaturated fatty acids (PUFAs) supplementation on plasma concentration of brain-derived neurotrophic factor (BDNF) and IL-6 which are important biochemical and immunological markers found in depression. Aims and Objectives: The aim of the current study was to assess the effect of supplementation of PUFA on MSG-induced depression in Wistar albino rats. Materials and Methods: The present prospective interventional study was conducted on 3-month-old, 24 male Wistar albino rats (weighing 200–300 g) for 21 days. The study group was divided into four equal groups among which 1st group that is control received distilled water with carboxymethylcellulose (CMC), the 2nd group positive control group received 500 mg of MSG along with CMC, the 3rd group normal control with PUFA received PUFA dissolved in CMC and the 4th group was positive control with PUFA received MSG dissolved in CMC and PUFA intervention was introduced from the 7th day. The study period was for 21 days and the 22nd day was an acclimatization day. The parameters in the blood samples of the rats were tested on the 23rd day using an ELISA kit and results were analyzed using Tukey’s post hoc test among the various groups and it was taken as statistically significant when the P < 0.05. Results: Among the groups, IL-6 levels raised and BDNF levels dropped in plasma of MSG-induced depressed rats. In PUFA-treated MSG-induced depressed rats, the plasma level of IL-6 was reduced and there was a significant rise in BDNF levels. Conclusion: PUFA supplementation is effective in treating MSG-induced depression in rats.
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Background: Food labelling is used as a tool to safeguard and promote public health by giving consumers accurate nutritional information to help them make informed dietary choices. Methods: This study was limited to the town panchayat and the village of Avinashi in the district Tirupur. A Questionnaire was used to collect data from 500 adult participants, on their knowledge, attitudes, and their sociodemographic profile. Results: Based on this study maximum number of subjects prefer monthly purchases in town 50% and in the village 46.66% of subjects and branded too. 410 subjects (82%) out of 500 were aware of manufacture and expiry. 100% were noted cost. Ingredients list was noted by 22% of respondents. About 12% did not check any other mandatory information while purchasing. 62% & 76.6% were aware of green and red symbols, while 16% of subjects were not aware. 22% of the subjects were not seen or aware of the nutritional values of the product. After the testing, the sample of masala showed the presence of monosodium glutamate in 11 samples which were unmentioned in the ingredients list. Hence it shows the food package label did not mention the ingredient added in the food masala. Conclusions: It is concluded that nutrition labelling is a useful tool for guiding people toward consuming wholesome foods. Encouraging the potential of nutrition labelling and health claims to promote health. Truthful and complete information allows value comparisons to be made among competing products. Ingredient labelling also helps people avoid foods to which they may be allergic.
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Background: Monosodium glutamate (MSG) is widely used as a flavor enhancer in food, known for its ability to modulate umami taste and improve overall food palatability. Despite its recognized benefits in the food industry, concerns about its safety and potential health effects have sparked widespread debate. This systematic review aims to provide an in-depth analysis of the molecular mechanisms underlying MSG’s flavor-enhancing properties, its role in food palatability, and the scientific evidence surrounding its health impacts. Objectives: To review the current state of knowledge regarding: 1. The molecular chemistry and mechanism of MSG in flavor modulation. 2. The role of MSG in enhancing food palatability and consumer preferences. 3. he safety assessments and potential health effects of MSG, including both benefits and concerns. 4. MSG’s future applications in food science, particularly in low-sodium formulations, food security, and geriatric nutrition. Materials and Methods: A comprehensive search of peer-reviewed literature was conducted using databases such as PubMed, Web of Science, and Google Scholar. Studies focusing on MSG’s chemistry, its application in food, sensory studies, and health-related research were included. Regulatory assessments from food safety agencies (FDA, WHO, EFSA) were also reviewed. Results: Flavor Modulation: MSG enhances the umami taste by interacting with specific glutamate receptors (T1R1/T1R3), contributing to a balanced flavor profile in various cuisines. It is especially effective in reducing the need for excess salt and fat in processed foods while maintaining palatability.Food Palatability: Sensory studies show that MSG significantly improves food satisfaction, particularly in low- sodium or low-fat products. Consumers often prefer MSG-enriched foods due to enhanced flavor perception and texture.Health Impacts: Regulatory bodies have classified MSG as safe for consumption, with no conclusive evidence linking it to neurotoxicity or adverse metabolic effects at typical dietary levels. Some studies suggest MSG may aid in reducing sodium intake and improving food palatability in special populations, such as the elderly.Public Perception: Despite the scientific consensus on its safety, public concerns remain, largely fueled by misconceptions about "Chinese Restaurant Syndrome" and misleading media reports. Conclusions: MSG plays a pivotal role in modern food science as a safe and effective flavor enhancer. While public concerns persist, scientific evidence supports its safety and potential health benefits when used appropriately. Further research should focus on long-term health effects, innovative applications in low-sodium food formulations, and educational initiatives to address public misconceptions about MSG.
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Background: Short-term use of monosodium glutamate (MSG) induces anxiety in animals. Due to the lack of stringent regulations for food supplements and increase in the use of MSG in the past decade, the long-term effects of MSG need to be evaluated. There is a scarcity of the literature on the chronic effects of MSG on anxiety, hence the present study. Since anxiety models require an intact motor function, motor function was also evaluated. Aims and Objectives: The aim of the study was to evaluate the long-term effects of intraperitoneal (i.p.) MSG on mice models of anxiety (social interaction) and motor function (accelerating rota rod). Materials and Methods: The present prospective interventional study was conducted on 40 adult male Swiss albino mice. Mice were randomly divided into four equal groups to receive, distilled water, and MSG at doses of 40, 60, and 80 mg/kg/day for 3 months. Parameters were assessed at baseline, 1 month, 2 months, and 3 months of daily MSG administration. Statistical tests of significance were the Wilcoxon signed-rank test and Friedman test (within group) and Kruskal–Wallis Test (between groups), P < 0.05 was considered statistically significant. Results: Social interaction time was reduced in all the MSG-treated groups (P < 0.05) without any change in motor function (P > 0.05). Anxiety was evident from 40 mg/kg/day MSG from the 1st month till 3 months compared to baseline and controls. Duration-dependent change in social interaction was observed with MSG at doses of 40 mg/kg/day and 60 mg/kg/day. Dose-dependent change in social interaction was not observed among treatment groups. Conclusion: Long-term administration of MSG produced anxiogenic effects at doses of 40 mg/kg, 60 mg/kg, and 80 mg/kg without impairing the motor functions in the mice.
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Background: Monosodium glutamate (MSG), a flavor enhancer, is one of the most widely used commercial food additives. MSG produces oxidative stress in various tissues including cerebellar cortex. There is a paucity if data on the histological and immunohistochemical changes of glial fibrillary acidic protein (GFAP) on chronic administration of MSG at doses equivalent to human consumption (i.e., 40 mg/kg, 60 mg/kg, and 80 mg/kg daily for 3-month duration), hence this study. Aims and Objectives: The aim of the study was to evaluate the histological and immunohistochemical effects produced by MSG at doses equivalent to human consumption (40mg/kg/day, 60 mg/kg/day, and 80 mg/kg/day) in cerebellar cortex of adult mice. Materials and Methods: Study commenced after the Institutional Animal Ethics Committee approval. 40 Swiss-albino mice were randomly divided into four groups. Group 1 served as the negative control and received distilled water i.p. Groups 2, 3, and 4 received MSG at increasing doses. Animals were euthanized at 3 months, cerebellar samples were examined histopathologically and immunohistochemically. Results: Degeneration of the layers of cerebellar cortex in histopathology and reduction in the GFAP activity was observed in immunohistochemistry. Conclusion: MSG due to its wide consumption can cause degenerative changes in the cerebellum.
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BACKGROUND:Inhibitory control and drug craving are the core elements of evaluating drug withdrawal in methamphetamine addicts,which has attracted much attention in academic circles.As we all know,in order to achieve complete abstinence from drug addiction,the key is to restore the damaged inhibition and control function of drug addicts and effectively reduce the craving for drugs. OBJECTIVE:To systematically analyze the relationship between exercise and methamphetamine abstinence inhibitory control and drug craving,to find out an effective exercise intervention scheme that can promote methamphetamine abstinence,and to further explore the internal mechanism of exercise,in order to provide theoretical support and applied reference for the future use of exercise in drug withdrawal. METHODS:CNKI,WanFang,VIP,Web of Science,and PubMed databases were searched for relevant literature using the keywords of"exercise,physical activity,methamphetamine,inhibitory function,craving,addiction"in Chinese and"sport*,exercise,methamphetamine,drug craving,executive function,addiction"in English.According to the inclusion and exclusion criteria,86 documents were finally included for review. RESULTS AND CONCLUSION:In terms of inhibitory control in methamphetamine abstinent individuals,either acute and long-term moderate-intensity aerobic exercise or acute high-intensity interval training can significantly improve the inhibitory control capacity of methamphetamine abstinent individuals.For long-term aerobic exercise,aerobic group exercise or full-body comprehensive exercise is more effective.If the exercise format is power cycling,it is recommended to increase the frequency of exercise intervention.In terms of the drug craving intensity in methamphetamine abstinent individuals,acute moderate-intensity aerobic exercise and resistance training,as well as long-term moderate-intensity,high-intensity,or progressive load aerobic and resistance training,can effectively reduce the drug craving in methamphetamine abstinent individuals.Exercise exerts intrinsic regulatory effects on methamphetamine-mediated addiction.Exercise can influence the expression of tyrosine hydroxylase in the brain's ventral tegmental area,thereby stimulating the expression of dopamine receptor coupling proteins and promoting dopamine synthesis in the brain's reward regions,thereby compensating for dopamine depletion caused by methamphetamine addiction.Furthermore,exercise can also regulate protein kinase A inhibitors,affecting the protein kinase A signaling pathway mediated by dopamine D1 receptors,by inhibiting protein kinase A,thus affecting cAMP response element-binding protein and regulating methamphetamine addiction.Additionally,exercise can also,at the genetic level,affect the expression of the c-fos gene in the brain's nucleus accumbens region,activate a subset of glutamatergic neurons in this area,generate a rewarding effect,and thus improve methamphetamine addiction.Although current research has confirmed the relationship between exercise and methamphetamine addiction and has clarified the brain mechanisms underlying the effects of exercise,whether there are other brain regulatory pathways for the effects of exercise remains to be explored through more scientifically rigorous animal or human experiments,starting from the cellular or molecular level.
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Most of the current research on depression focuses on neuronal regulation,while the astrocytic mechanism of depression is far from explored.Astrocytes are the most numerous and widely distributed glial cells in the central nervous system.With a complex structural morphology,astrocytes play an important role in a variety of neuropsychiatric disorders by interacting with neuronal synapses,vasculature and other glial cells.Recent studies have shown that astrocytes may be involved in depression by regulating monoamine transmitters,glutamate cycle,synaptic plasticity,energy metabo-lism,and neuroinflammation.This review is intended to inspire new ideas for the treatment of depres-sion and the development of novel drugs based on astrocyte regulation.
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Objective To observe the effects of electroacupuncture(EA)on glutamate(Glu),metabotropic glutamate receptor 2/3(mGluR2/3)and apoptosis related proteins expression in hippocampus in rats with acute myocardial ischemia(AMI);To explore the mechanism of EA against AMI.Methods Totally 50 SD rats were randomly divided into sham-operation group,model group,EA group and inhibitor group,with 10 rats in each group.Except for the sham-operation group,the rats were treated with ligation at the left anterior descending coronary artery to establish AMI model.The rats in the EA group was treated with EA at"Shenmen"and"Tongli",30 minutes each time,once a day for 3 consecutive days.The rats in the inhibitor group were treated with injection of LY341459 via the lateral ventricle 30 min after modeling.HE staining was used to observe myocardial tissue morphology,and ELISA was used to detect Caspase-3 activity in myocardial tissue and Glu content in hippocampal tissue,immunofluorescence staining was used to detect mGluR2/3 expression in hippocampal tissue,TUNEL staining was used to detect apoptosis in hippocampal tissue cells,Western blot was used to detect the expressions of PI3K,Akt,and Caspase-3 protein in hippocampal tissue.Results Compared with the sham-operation group,the myocardial cells of the model group rats showed sparse and swelling with severe infiltration of inflammatory cells;the activity of Caspase-3 in myocardial tissue significantly increased,and the Glu content,positive expression of mGluR2/3,number of apoptotic cells in hippocampal tissue significantly increased(P<0.01),and the expressions of PI3K and Akt proteins in hippocampal tissue were significantly decreased,while the expression of Caspase-3 protein significantly increased(P<0.01).Compared with the model group,myocardial cell edema and inflammatory cell infiltration were reduced in the EA group and inhibitor group,the activity of Caspase-3 in myocardial tissue was significantly decreased,the Glu content,positive expression of mGluR2/3,and number of apoptotic cells in hippocampal tissue were significantly reduced(P<0.01),the expressions of PI3K and Akt proteins in hippocampal tissue significantly increased,while the expression of Caspase-3 protein significantly decreased(P<0.01).Conclusion EA can improve myocardial injury in AMI rats,and its mechanism may be related to activation of PI3K/Akt signaling pathway,inhibition of hippocampal mGluR2/3 overexpression,reduction of Glu accumulation,inhibition of apoptosis of hippocampal neurons and reduction of neurotoxicity.
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Objective To explore the correlation of serum glutamate(Glu)and gamma-aminobutyric acid(GABA)levels with clinical symptoms in chronic schizophrenia patients,and to assess their diagnostic value for cognitive impairment.Methods A total of 92 patients with chronic schizophrenia and another 80 healthy individuals in Wuhan Mental Health Center/Wuhan Hospital for Psychotherapy from January 2021 to July 2022 were enrolled as study group and control group,respectively.The patients in the study group were divid-ed into the cognitive impairment group(44 cases)and the cognitive normal group(48 cases)according to Montreal Cognitive Assessment Scale(MoCA).Clinical symptoms were assessed by using Positive and Nega-tive Syndrome Scale(PANSS).MoCA was used to evaluate the cognitive function.The levels of Glu and GA-BA in plasma were determined by high-performance liquid chromatography/electrospray tandem mass spec-trometry.The scores of PANSS and MoCA as well as serum levels of Glu and GABA were compared between two groups.Then the correlation of serum Glu and GABA levels with clinical symptoms and the diagnostic value for cognitive impairment in the patients in the study group were investigated.Results The Glu level in the study group was higher than that in the control group,and the GABA level was lower than that in the con-trol group(P<0.05).The serum Glu levels in both the cognitive impairment group and the cognitive normal group were higher than the normal range,and the Glu level in the cognitive impairment group was higher than that in the cognitive normal group(P<0.05).The serum GABA levels in both the cognitive impairment group and the cognitively normal group were lower than the normal range,and the GABA level in the cogni-tive impairment group was lower than that in the cognitive normal group(P<0.05).In the study group,ser-um Glu level was positively correlated with negative,positive,general psychopathological symptom scores,and overall score in PANSS(P<0.05),while GABA level was negatively correlated with negative,positive,gener-al psychopathological symptom scores,and overall score in PANSS(P<0.05).The sensitivity of the single and combined detection of serum Glu and GABA for the diagnosis of cognitive impairment in patients with chronic schizo-phrenia was 77.3%,72.7%and 93.2%,respectively,and the specificity was 72.9%,72.9%,and 75.0%,respec-tively,and the area under the curve was 0.778,0.769,and 0.868,respectively.Conclusion Serum Glu level in patients with chronic schizophrenia is higher than that in healthy individuals,while GABA level is lower than that in healthy individuals,and the above two indicators are correlated with PANSS score,which have high value in diagnosing cognitive impairment and could be used as effective biological indicators to help clinical doctors judge patients'cognitive function.
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting both upper and lower motor neurons. ALS patients develop progressive muscle atrophy, muscle weak and paralysis, finally died of respiratory failure. ALS is characterized by fast aggression and high mortality. What' s more, the disease is highly heterogeneous with unclear pathogenesis and lacks effective drugs for therapy. In this review, we summarize the main pathological mechanisms and the current drugs under development for ALS, which may provide a reference for the drug discovery in the future.
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Objective To observe the expression and localization of group Ⅰ metabotropic glutamate receptors (mGluR1/ 5) in rat superior cervical ganglion (SCG) and the effect of chronic intermittent hypoxia (CIH) on mGluR1/ 5 protein level. Methods Twelve male SD rats were randomly divided into control group(Ctrl)and CIH group(CIH), 6 rats in each group. After 6 weeks of modeling, the effect of CIH on mGluR1/ 5 protein level was detected by Western blotting, the expression and distribution of mGluR1/ 5 in SCG were detected by immunohistochemistry and double-immunofluorescent staining. Results mGluR1/ 5 was expressed in rat SCG. mGluR1 was distributed in neurons and small intensely fluorescent (SIF) cells, but not in satellite glial cells (SGCs), nerve fibers and blood vessels, whereas mGluR5 was mainly distributed in nerve fibers and a little in neurons, but not in SGCs, SIF cells and blood vessels. CIH increased the protein levels of mGluR1/ 5 (P<0. 01) in rat SCG. Conclusion Both mGluR1 and mGluR5 are expressed in the rat SCG, but their distribution are different, and the increased protein levels of both may be involved in CIH-induced hypertension.
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Objective To investigate the effect of cholecystokinin octapeptide(CCK-8)on glutamate transporter 1(GLT-1)expression in hippocampal astrocytes induced by glutamate(Glu).Methods The mouse hippocampal astrocytes were isolated and the toxicity of CCK-8 at different concentrations on the mouse hippocampal astrocytes was detected.The cells were divided into control group,Glu group,Glu+0.1 μmol/L CCK-8 group,Glu+0.5 μmol/L CCK-8 group and Glu+1.0 μmol/L CCK-8 group.MTT assay was used to detect cell proliferation.Flow cytometry was used to detect cell apoptosis.Biochemical kit was used to detect Glu content in the extracellular supernatant,and qRT-PCR was used to detect the mRNA expression of GLT-1 and glutamate/aspartate transporter(GLAST).The protein expressions of Caspase-3,Bcl-2,GLT-1 and GLAST were detected by Western blotting,and the expression of TNF-α in the cell supernatant was detected by ELISA.Results CCK-8 at different concentrations had no significant effect on the proliferation of mouse hippocampal astrocytes.Compared with the control group,the cell proliferation ability and the expression levels of Bcl-2 protein,GLT-1 and GLAST mRNA and protein in Glu group were significantly decreased(all P<0.01),the apoptosis rate,extracellular Glu content,Caspase-3 protein expression level in cells and TNF-α level in cell supernatant were significantly increased(all P<0.01);Compared with the Glu group,the cell proliferation a-bility and the expression levels of Bcl-2 protein,GLT-1 and GLAST mRNA and protein in the Glu+0.5 μmol/L CCK-8 group and Glu+1.0 μmol/L CCK-8 group were significantly increased(all P<0.05),the apoptosis rate,extracellular Glu content,Caspase-3 protein expression level in cells and TNF-α level in cell supernatant were significantly decreased(all P<0.01).Con-clusion CCK-8 can inhibit Glu-induced inflammatory response of astrocytes,promote the expression of GLT-1,reduce the con-centration of extracellular Glu,promote cell proliferation and inhibit apoptosis.
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Introducción: El glutamato monosódico se emplea en humanos desde el pasado siglo como potenciador del sabor. Su inoculación parenteral en murinos durante el período neonatal causa lesiones en varios núcleos hipotalámicos. Objetivo: Describir los efectos del glutamato monosódico sobre el sistema neuroendocrinoinmune en murinos. Metodos: Se realizó una revisión de artículos de libre acceso en las bases de datos PubMed y SciELO entre enero de 2013 y julio de 2020. También se examinó el texto básico de la asignatura Sangre y Sistema Inmune de la carrera de medicina. Desarrollo: Con independencia de su efecto adictivo, varios estudios defienden la inocuidad del glutamato monosódico. Sin embargo, este compuesto puede atravesar la barrera hematoencefálica de neonatos de murinos, y ocasionar trastornos metabólicos, reproductivos y del sistema inmune. Conclusiones: El glutamato monosódico en roedores causa alteraciones en los órganos que integran el suprasistema neuroendocrinoinmune y, por tanto, afecta sus funciones homeostáticas. Los mecanismos patogénicos no se conocen con exactitud.
Introduction: Monosodium glutamate has been used in humans since the last century as a flavor enhancer. Its parenteral inoculation in murine during the neonatal period causes lesions in several hypothalamic nuclei. Objective: To describe the effects of monosodium glutamate on the neuroendocrine immune system in murine samples. Methods: A review of open access articles in the PubMed and SciELO databases was conducted between January 2013 and July 2020. The basic text of the Blood and Immune System course of the medical school was also reviewed. Development: Regardless of its addictive effect, several studies defend the safety of monosodium glutamate. However, this compound can cross the blood-brain barrier of murine neonates, causing metabolic, reproductive and immune system disorders. Conclusions: Monosodium glutamate in rodents causes alterations in the organs that make up the neuroendocrine-immune suprasystem and, therefore, affects their homeostatic functions. The pathogenic mechanisms are not known exactly.
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Background: Medications currently used to treat pain are frequently associated with serious adverse effects and rapid development of tolerance. Thus, there is a need to develop more effective, and safer medicines for the population. Blocking NMDA receptors (NMDAR) has shown to be a promising target for the development of new drugs. That statement is due to NMDAR activation and glutamate release in the spinal cord which affects chronic pain modulation. Therefore, the aim of this study was to evaluate the possible spinal antinociceptive activity of PnTx4(5-5) toxin. The peptide is purified from the venom of the spider P. nigriventer and its affinity for NMDAR and sodium channels Nav1.2-1.6 has already been established. Methods: We compared its effect and safety with MK-801 (NMDAR antagonist) and evaluated its influence on glutamate and reactive oxygen species (ROS) levels in CSF. PnTx4(5-5) was administered intrathecally in the Formalin test and co-administered with NMDA in the Spontaneous pain test. After three minutes of observation, mice cerebrospinal fluid was collected to measure glutamate and ROS levels. Results: The spider peptide inhibited nociception as post-treatment in the inflammatory phase of the Formalin test. Furthermore, it inhibited spontaneous nociception induced by NMDA, being more potent and effective than MK-801 in both models tested. A glutamate rise level in the CSF of mice was significantly reduced by the toxin, but ROS increase was not affected. The animals' motor skills were not affected by the tested doses of NMDAR inhibitors. Conclusion: In conclusion, the results suggest PnTx4(5-5) may mediate its antinociceptive effect in the spinal cord not only by inhibiting postsynaptic receptors but probably also by acting on autoreceptors. This effect does not affect the motricity of mice at the highest dose tested, which suggests that it has therapeutic potential and safety for use as a painkiller.
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Spider Venoms , Spinal Cord , Dizocilpine Maleate , Receptors, N-Methyl-D-Aspartate , AnalgesicsABSTRACT
Background: Sodium mono glutamate (MSG), the sodium salt of glutamic acid, is a food flavoring agent that is widely used in many countries. Pomegranate is used as a traditional medication in numerous countries, it is planted in Asian countries, Mediterranean countries and the U.S.A. Aim of the work: The present study aimed to detect structural and functional changes in adult rat kidney tissue treated with sodium mono glutamate, and the possible protective effect of pomegranate on the kidney treated with MSG. Materials and Methods: This study was done by using 60 adult Wistar Albino rats of both sexes were divided into three equal groups: Group I (control group), Group II (sodium mono glutamate treated group), and Group III (combined MSG and pomegranate treated group) Doses were given once daily for 8 weeks every day. At the end of the treatment period, blood samples collected from each rat were used for measuring the values of urea and creatinine. Also animals of the different groups were sacrificed at the end of the experiment, quickly dissected and the kidneys were removed and stained with hematoxylin and eosin (H&E) for the histological examination by light microscopy, other tissue sections were evaluated using a transmission electron microscope. Both were used to examine the effect of sodium mono glutamate on cortex of the kidneys of albino rats ,compared with control group and the combined MSG and pomegranate group. Results: There was a major rise in blood urea level and blood creatinine level in sodium mono glutamate treated group in contrast to the control group. There was a significant reduction in blood urea level and blood creatinine level in combined sodium mono glutamate and pomegranate treated group in comparison to MSG treated group. Examination of kidney tissue of rats treated with sodium mono glutamate (Group. II) showed damaging changes of its structure. The glomerulus had markedly widened blood capillaries with thickened filtration membrane. The epithelial tubular cells had marked degenerative changes. Examination of rats kidney tissue treated with sodium mono glutamate and pomegranate (Group III) revealed improvement of the lesions in the glomeruli and renal tubules. Conclusion: Pomegranate protected the kidneys and restricted the histological and functional alterations caused by sodium mono glutamate, and thus, there is an advantage of usage of pomegranate with sodium mono glutamate.
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Este estudio tuvo como objetivo demostrar la existencia de variaciones morfológicas en el tejido conectivo de la glándula submandibular de ratas obesas expuestas a glutamato monosódico (GMS). Se utilizaron 12 ratas Sprague Dawley machos recién nacidas (6 ratas para el grupo 1, control; 6 ratas para el grupo 2 (GMS), 4 mg/g de glutamato monosódico de peso (5 dosis) mantenidas por 16 semanas respectivamente con una dieta y agua ad libitum. En el estudio se realizó un análisis estereológico e histológico, demostrándose una variación en el tejido conectivo presentando una disminución del volúmen glandular, mayor fibrosis, y disminución de adipocitos a nivel periférico siendo reemplazado por tejido rico en colágeno. Los vasos sanguíneos observados a nivel estereológico no presentan mayores cambios en cuanto a volumen, superficie y área.
SUMMARY: This study aims to demonstrate the existence of morphological variations in the connective tissue of the submandibular gland of obese rats exposed to MSG. Twelve male newborn Sprague Dawley rats were used (6 rats for group 1, control; 6 rats for group 2 (MSG), 4 mg/g of monosodium glutamate of weight (5 doses) maintained for 16 weeks respectively with a diet and water ad libitum. In the study, a stereological and histological analysis was carried out, demonstrating a variation in the connective tissue, presenting a decrease in the glandular volume, greater fibrosis, and a decrease in adipocytes at the peripheral level, being replaced by tissue rich in collagen. Blood cells observed at the stereological level do not present major changes in terms of volume, surface and area, but in the histological study greater vascularization is observed.
Subject(s)
Animals , Male , Rats , Sodium Glutamate/administration & dosage , Submandibular Gland/drug effects , Obesity , Sodium Glutamate/pharmacology , Blood Vessels/drug effects , Body Weight , Fibrosis , Rats, Sprague-Dawley , Connective Tissue/drug effects , Animals, NewbornABSTRACT
Abnormal homeostasis of glutamate(Glu)and γ-aminobutyric acid(GABA)in the brain is one of pathophysiological mechanisms of brain dysfunction in major depressive disorder(MDD).Neurotransmitters play an important role in maintaining chemical balance in the brain,and pharmacological and non-pharmacological therapies based on resetting excitation-inhibitory neurotransmitter system rebalancing are of interest.Studies based on magnetic resonance spectroscopy(MRS)have shown a homeostasis imbalance of Glu and GABA in the brain of MDD patients.Pharmacological therapies such as ketamine,selective serotonin reuptake inhibitors,and other novel receptor modulators and non-pharmacological therapies such as repetitive transcranial magnetic stimulation,electroconvulsive therapy,and physical exercise can target on the regulation of neurotransmitter levels.Abnormal homeostasis of Glu and GABA provides theoretical support for revealing pathophysiologic mechanisms of MDD,exploring neurotransmitter biomarkers,guiding clinical practice and facilitating personalized treatment.
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Depression is one of the most common psychiatric disorders with high prevalence, disability and relapse rates, and its etiology and pathogenesis are complex and still not fully understood. Neurotransmitters play a key role in maintaining chemical homeostasis in brain, and many studies have shown a strong link between neurotransmitters and the development and treatment of depression in recent years. Therefore, studying the neurotransmitters associated with depression has the potential to provide research targets and ideas for the pathogenesis and treatment strategies of depression. This paper reviews the recent domestic and foreign research results on neurotransmitter function and the pathogenesis of depression, aiming to analyze the in-depth relationship between neurotransmitter function and the pathogenesis of depression, and provide research ideas for the follow-up ex-ploration of the pathogenesis and diagnosis and treatment strategies of depression.
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Many efforts have been made to understand excitotoxicity and develop neuroprotectants for the therapy of ischemic stroke. The narrow treatment time window is still to be solved. Given that the ischemic core expanded over days, treatment with an extended time window is anticipated. Bestrophin 1 (BEST1) belongs to a bestrophin family of calcium-activated chloride channels. We revealed an increase in neuronal BEST1 expression and function within the peri-infarct from 8 to 48 h after ischemic stroke in mice. Interfering the protein expression or inhibiting the channel function of BEST1 by genetic manipulation displayed neuroprotective effects and improved motor functional deficits. Using electrophysiological recordings, we demonstrated that extrasynaptic glutamate release through BEST1 channel resulted in delayed excitotoxicity. Finally, we confirmed the therapeutic efficacy of pharmacological inhibition of BEST1 during 6-72 h post-ischemia in rodents. This delayed treatment prevented the expansion of infarct volume and the exacerbation of neurological functions. Our study identifies the glutamate-releasing BEST1 channel as a potential therapeutic target against ischemic stroke with a wide time window.
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Objective:To investigate the expression of phosphorylated glutamate receptor 2[p-GluR2(S880)]in oligodendrocyte precursor cells(OPCs)of mice model of hypoxic ischemic brain injury(HIBI).Methods:The HIBI model of C57BL/6 neonatal mice was established by right common carotid artery ligation and hypoxia for 90 min.The anxiety-like behavior of the mice was evaluated by elevated plus maze(EPM)and open field test(OFT).The expres-sion of p-GluR2(S880),oligodendrocyte marker 4(O4)and myelin basic protein(MBP)in brain tissue of HIBI model mice was detected by immunofluorescence staining.What's more,the expression levels of p-GluR2(S880)and MBP were detected by Western Blot.Results:Compared with sham operation group,there were significant anxiety-like behaviors 90 days after HIBI operation(P<0.05).The expression of MBP protein decreased significantly in 14 and 28 days after HIBI operation.The expression of p-GluR2(S880)protein was up-regulated at all time points after HIBI op-eration(P<0.05),and the number of O4 and p-GluR2(S880)double positive cells in brain tissue of HIBI group was significantly increased(P<0.05).Conclusion:The up-regulation of p-GluR2(S880)expression in OPCs may lead to myelination disorder in HIBI model mice.