Protective Effect of Syringaresinol on Excitatory Damage Induced by Sodium Glutamate in SH-SY5Y Cells / 中国实验方剂学杂志

Objective: To establish a model for the injury of human neuroblastoma cell (SH-SY5Y) induced by sodium glutamate, and to observe the protective effect of syringaresinol on cell damage from Viscum liquidambaricolum hayataon, and to explore its mechanism. Method: Construction of SH-SY5Y cell injury model using sodium glutamate.The experiment was divided into normal cell group, injury model group (sodium glutamate 50 mmol·L-1, sodium glutamate 50 mmol·L-1 + DMSO),syringaresinol experimental group (6.25, 12.5, 25 μmol·L-1), by cell counting, cell morphology observation, Annexin V-FITC/PI apoptosis detection, ROS reactive oxygen species detection, mitochondrial membrane potential, and Western blot, evaluation of syringaresinol on glutamate-induced neuronal excitability injury neuroprotective activity. Result: Compared with normal group, the cell survival rate of the model group was significantly decreased (PPPPP-1) showed a concentration-dependent increase in cells. Survival rate (PPPPPConclusion: Syringaresinol has significant protective activity against excitatory damage induced by sodium glutamate in SH-SY5Y neurons, the mechanism may be through anti-oxidative stress, repairing mitochondrial function and DNA damage to significantly reduce sodium glutamate-induced neuronal apoptosis.

Establishment and application value of a monosodium glutamate-rat-liver regeneration model / 临床肝胆病杂志

The establishment of an animal model of liver regeneration in a state of neuro-endocrine-immune network dysfunction is an urgent need to promote the research on the regulatory mechanism of liver regeneration. The monosodium glutamate (MSG)-rat-liver regeneration model is a composite model of liver regeneration which combines the MSG-rat model with the model of partial hepatectomy (PHx) or hepatotoxicity (for example, CCl4), and it is mainly used to investigate liver regeneration and its regulatory mechanism in the state of neuro-endocrine-immune network dysfunction, mechanisms and drug screening of liver-brain syndrome, and mechanisms of disease-syndrome combination and drug efficacy. Dysregulated liver regeneration process is observed in the MSG-rat-liver regeneration model established by the MSG-rat model and PHx, which is significantly different from the liver regeneration process in normal rats after major hepatectomy. The MSG-rat-liver regeneration model established by the MSG-rat model and hepatotoxicity has a significantly higher degree of liver fibrosis than normal rats with CCl4-induced liver fibrosis. The hypothalamic-pituitary-hepatic axis is an important mechanism of the influence of the external environment on liver regeneration, and the imbalance of epithelial-mesenchymal transition/mesenchymal-epithelial transition is an important mechanism of the influence of intrahepatic microenvironment on abnormal liver regeneration (liver fibrosis). The research on MSG-rat-liver regeneration model preliminarily reveals the efficacy and mechanism of traditional Chinese medicine in the prevention and treatment of liver and related diseases (including liver-brain syndrome) by influencing the neuro-endocrine-immune-liver regeneration regulatory network and promotes the research on the combination of diseases and syndromes. The establishment and application of the MSG-rat-liver regeneration model has important scientific significance and application value in further exploration of the complex mechanism of liver regeneration and the mechanism of traditional Chinese medicine in regulating liver regeneration.

Estandarización de un modelo para inducir obesidad en ratas / Standardization of model to induce obesity in rats

Fundamento: La obesidad es un factor de riesgo para múltiples enfermedades. Existen diversos modelos en ratas para inducir obesidad. Los modelos genéticos y la obesidad inducida por la dieta son costosos. Dentro de los modelos hipotalámicos de obesidad está el que se logra mediante la administración de glutamato monosódico en período neonatal. Esta sustancia no es costosa y produce las alteraciones metabólicas más importantes que se ven en la obesidad humana. Objetivo: seleccionar un esquema de tratamiento adecuado para inducir obesidad con glutamato monosódico en ratas Wistar en periodo neonatal. Métodos: se administró glutamato monosódico a ratas Wistar en período neonatal, siguiendo tres esquemas diferentes de tratamiento (con cinco, siete y diez dosis), a 4mg/g/día, y mediante dos vías de administración: subcutánea e intraperitoneal. A los controles se les administró cloruro de sodio al 0,9 %. Para realizar el diagnóstico de obesidad, a los 90 días se evaluaron las variables: peso, longitud hocico-ano e índice de Lee. Resultados: con todos los esquemas de tratamientos ensayados, la longitud hocico-ano resultó diferente estadísticamente entre el grupo tratado con glutamato monosódico y los controles. El 100 % de las ratas que alcanzaron la adultez, inyectadas con glutamato monosódico, se hicieron obesas. Conclusión: el esquema con cinco dosis de glutamato monosódico, aplicado en días alternos por vía subcutánea, fue seleccionado por desarrollarse la obesidad con menor manipulación y menor porcentaje de muertes neonatales.

Background: Obesity is a risk factor for multiple diseases. There are various rat models to induce this condition. Genetic models and diet-induced obesity are expensive. Within the models of hypothalamic obesity, there is one achieved by the administration of monosodium glutamate during the neonatal period. This substance is not expensive and causes the major metabolic alterations observed in human obesity. Objective: to select an appropriate treatment scheme to induce obesity with monosodium glutamate during neonatal period. Methods: monosodium glutamate was administered to Wistar rats during the neonatal period, using three different treatment schemes (with five, seven and ten doses) of 4mg/g/day through two routes of administration: subcutaneous and intraperitoneal routes. Controls were administered 0.9% sodium chloride. To establish the diagnosis of obesity, the following variables were measured at 90 days: weight, snout-anus length and Lee index. Results: with all treatment schemes tested, snout-anus length was statistically different between the group treated with monosodium glutamate and the controls group. 100% of the rats that reached adulthood injected with monosodium glutamate was obese. Conclusion: the scheme of five doses of monosodium glutamate, applied subcutaneously on alternate days, was selected as obesity is obtained with less handling and lower percentage of neonatal deaths.

Efeito da sobreposição de um modelo de obesidade neuroendócrina experimental e hipertensão arterial sobre a pressão arterial, peso corporal e parâmetros metabólicos e renais de ratos / Effects of the overlapping between an experimental model of neuroendocrine obesity with arterial hypertension under blood pressure, body weight and metabolic and renal parameters in rats

INTRODUÇÃO: A elevação do índice de massa corporaleapresençadesíndromemetabólica se associam com diminuição da função renal e o aparecimento de doença renal terminal. OBJETIVO: Avaliar o efeito da sobreposição de um modelo de obesidade experimental e hipertensão arterial sobre a pressão arterial, peso corporal e parâmetros metabólicos e renais de ratos. MÉTODOS: Foram estudados ratos machos das cepas Wistar e espontaneamente hipertensos (SHR). Os grupos MSG receberam glutamato monossódico no período neonatal (WST + MSG e SHR + MSG). Os animais controles receberam salina no período neonatal (WST e SHR). Após completarem três meses de vida, por 12 semanas foram pesados e tiveram a pressão arterial de cauda aferida semanalmente. A determinação de microalbuminúria foi realizada nas semanas 0, 4, 8 e 12. Ao final do período de acompanhamento, coletou-se sangue para glicemia de jejum, creatinina e perfil lipídico. Os rins foram retirados, corados e o índice de esclerose glomerular foi calculado. RESULTADOS: A administração de MSG produziu maior ganho percentual de peso corporal, elevação da glicemia de jejum e maior grau de lesão glomerular nos ratos WST -MSG e SHR -MSG quando comparados aos seus controles. Houve maior excreção urinária de albumina nos ratos do Grupo SHR + MSG quando comparados aos SHR. Não houve diferença estatística na pressão arterial de cauda, creatinina e parâmetros do metabolismo lipídico. CONCLUSÕES: A associação de obesidade neuroendócrina e a hipertensão arterial promoveram alterações morfológicas e funcionais no glomérulo mais severas do que aquelas observadas nos ratos somente hipertensos.

INTRODUCTION: Increased body mass index and the metabolic syndrome are associated with decreased renal function and the development of end-stage kidney disease. OBJECTIVE: To evaluate the effect of the overlap between an experimental model of obesity and genetic hypertension on the blood pressure, body weight and metabolic and kidney parameters of rats. METHODS: We studied male rats of the Wistar (WST) and spontaneously hypertensive rats (SHR) strains. Monosodium glutamate (MSG) was administered in the neonatal period to both strains, to make up two groups: WST + MSG and SHR + MSG. Animals in the control groups (WST and SHR) received saline. After completing three months of life, a 12-week follow-up period ensued, during which bi-weekly measurements of body weight (BW) and tail-cuff blood pressure (TCBP) were obtained. Microalbuminuria was analyzed at weeks 0, 4, 8 and 12. At the end of the follow-up period, blood was obtained for fasting glucose, plasma creatinine, and lipid profile determinations. The kidneys were removed, stained, and the glomerular sclerosis index was calculated. RESULTS: The administration of MSG produced higher percentage body weight gain, higher fasting blood glucose and a higher degree of glomerular injury in WST-MSG and MSG-SHR rats, compared to their controls. Greater urinary albumin excretion was observed in SHR + MSG rats, when compared to SHR. There was no statistical difference in the TCBP, creatinine, and lipid profile. CONCLUSIONS: The association of neuroendocrine obesity and arterial hypertension promoted morphological and functional changes in the glomerulus. These changes were more severe than those observed in hypertensive-only rats.

Effect of the oral administration of monosodium glutamate during pregnancy and breast-feeding in the offspring of pregnant Wistar rats / Efeito da administração de glutamato monossódico durante a gestação e amamentação na prole de ratas Wistar prenhes

PURPOSE: Determine the effects of the MSG (monosodium glutamate) in the offspring of pregnant rats through the comparison of the weight, NAL (nasal-anal length) and IL (Index of Lee) at birth and with 21 days of life. METHODS: Pregnant Wistar rats and their offspring were divided into 3 groups: GC, G10 and G20. Each of the groups received 0 percent, 10 percent and 20 percent of MSG, respectively from coupling until the end of the weaning period. RESULTS: Neither weight nor NAL were different among the groups at birth. The group G20 at birth had an IL lower than the group GC (p<0,05) and with 21 days of life presented weight and NAL lower than the groups G10 and this lower than the GC (p<0,01). Otherwise the G20 at 21 days of life had the IL similar to the other two groups. The weight profit percentage from birth to the 21st day of life was lower in the G20 regarding the other two groups (p<0,01). The G20 had a NAL increase percentage from birth to the 21st day of life lower than the G10 and this lower than the GC (p<0,01). CONCLUSIONS: MSG presented a dose-dependent relation in the variables weight and NAL. It caused a decrease in the growth pattern as well as in the weight gain pattern until the 21st day of life. The IL of the group 20 percent had an increased in relation to the control group after 3 weeks of follow up.

OBJETIVO: Avaliar o efeito do glutamato monossódico (GMS) nos fetos de ratas prenhes por meio da comparação do peso, comprimento nasal-anal (CNA) e índice de Lee (IL) ao nascimento e com 21 dias de vida. MÉTODOS: Foram utilizadas ratas prenhes da linhagem Wistar distribuídas em três grupos: grupo controle (GC), G10 e G20. Estes, respectivamente, foram alimentados com ração contendo 0, 10 e 20 por cento de GMS desde o período de acasalamento até o final da amamentação. RESULTADOS: O peso e o CNA não foram diferentes entre os grupos ao nascimento. O grupo G20, ao nascimento, teve IL menor que o grupo GC (p < 0,05) e, aos 21 dias de vida, apresentou peso e CNA menores que o grupo G10, o qual foi menor que o GC (p < 0,01). O grupo G20, aos 21 dias de vida, teve IL semelhante aos outros dois grupos. O percentual de ganho de peso do nascimento ao 21º dia de vida foi menor no G20 em relação aos outros dois grupos (p < 0,01). O grupo G20 teve percentual de aumento de CNA do nascimento ao 21º dia de vida menor que o grupo G10, e este menor que o grupo GC (p < 0,01). CONCLUSÕES: O GMS nas concentrações de 10 e 20 por cento na ração de ratas prenhes Wistar apresentou uma relação dose-dependente nas variáveis peso e CNA. Houve diminuição no padrão de ganho de peso e de aumento de CNA do nascimento ao 21º dia de vida com uso de GMS. O IL na prole do grupo G20 aumentou em relação ao do grupo GC após 3 semanas de acompanhamento.

Study of animal model of hypertensive disorder complicating pregnancy in pregnant rats stimulated by homocysteine and monosodinm glutamate / 中华妇产科杂志

Objective To determine whether homocysteine(Hcy)and monosodium glutamate (MSG)could lead to animal model of hypertensive disorder complicating pregnancy and its mechanism. Methods Female adult Wistar rats were randomly divided into 4 groups:pregnant control group(PN), pregnant Hcy group(PH),pregnant glutamic acid group(PG)and pregnant Hcy and glutamie acid group (PHG).The rats of each group were injected with Hey 200 mg/kg or physiological saline every day intraperitoneally and with MSG or 0.9% saline every other day via Hcy injection from the 10th day to the 20th day of pregnancy.The blood pressure,urine protein,function of liver and kidney,weight of placenta, length and weight of fetus were all measured.The histological change of the pallium and the change of behavior of pregnant rats were also observed.Results(1)The blood pressure in PH[(107?8)mm Hg, 1 mm Hg=0.133 kPa],and PHG group [(109?10)mm Hg] after the treatment increased significantly compared with those in other groups from the 12 th day after pregnancy(P

The effect of injection repeatedly of monosodium glutamate on the body temperature in rabbits / 中国病理生理杂志

Further study of the effect of monosodium glutamate on body temperature using rabbits as experimental model by repeatedly intravenous injection of MSG. The experimental results showed that the body temperature of rabbits were decreased significantly at a time of each day consecutively for three days with medium dose MSG(0.5g/kg/day) However, this effect was disappeared following the fourth administration of MSG a week later, and so did the fifth administration of MSG two weeks later. Those results suggested that the disappearance of decreased body temperature by MSG may be due to tolerance development after MSG was administrated repeatedly. The authors proposed two hypotheses of mechanisms for the development of MSG"tolerance". which would be investigated further.

Study on the effect of monosodium glutamate on the body temperature and its mechanism in rabbit / 中国病理生理杂志

With 58 of New Zeeland rabbits, following experiments were carried out: (1) the dose-response relationship of MSG which decreased the body temperat ure; (2) the effects of the propranolol and the anisodamine (654-2) on the action of decreasing body temperature by MSG. The results indicated: following intravenous administration of MSG at a dose of 0.5g/kg. w and 1.0g/kg. w, the body temperature of rabbits were decreased significantly, but at a dose of 0.1g/kg.w, the change of temperature was insignificant.Pretreatment with propranolol did not affect the effect of MSG decreasing body temperature which was blocked significantly by anisodamine, one of blocker of the cholinergic nerve. The authors suggest that the effect of MSG decreasing body temperature may depend on the cholinergic nerve.