Monosodium Glutamate Induced Research Articles

Protective and/or Therapeutic Effects of Curcumin Nanoparticles on Monosodium Glutamate Induced Cardiotoxicity in Male Albino Rats

Protective and/or Therapeutic Effects of Curcumin Nanoparticles on Monosodium Glutamate Induced Cardiotoxicity in Male Albino Rats

Impairment of Insulin Signalling Pathway: AMPKα/SIRT1 and Pathophysiological Involvement of Gut Microbiota in Monosodium Glutamate Induced Polycystic Ovary Syndrome with Palliative Role of Flaxseed.

Impairment of Insulin Signalling Pathway: AMPKα/SIRT1 and Pathophysiological Involvement of Gut Microbiota in Monosodium Glutamate Induced Polycystic Ovary Syndrome with Palliative Role of Flaxseed.

The Impact of Alpha-lipoic acid on the Monosodium Glutamate Induced Motor Coordination Dysfunction in Rats

The Impact of Alpha-lipoic acid on the Monosodium Glutamate Induced Motor Coordination Dysfunction in Rats

Potential Ameliorative Effect of Crude Honeybee on Monosodium Glutamate Induced Nephrotoxicity to Male Rats

Potential Ameliorative Effect of Crude Honeybee on Monosodium Glutamate Induced Nephrotoxicity to Male Rats

Anti-oxidant and Hepatoprotective Possibilities of Lycopene against Monosodium Glutamate Induced Detrimental Effects in Rats

Anti-oxidant and Hepatoprotective Possibilities of Lycopene against Monosodium Glutamate Induced Detrimental Effects in Rats

Ameliorative Effect of Jojoba Oil on Monosodium Glutamate Induced Cardiotoxicity and Neurotoxicity: Molecular, Metabolic and Histopathological study

Ameliorative Effect of Jojoba Oil on Monosodium Glutamate Induced Cardiotoxicity and Neurotoxicity: Molecular, Metabolic and Histopathological study

Potential Aphrodisiac Effect of Ginkgo Biloba in Monosodium Glutamate Induced Reproductive Behavior Changes in Mice

Potential Aphrodisiac Effect of Ginkgo Biloba in Monosodium Glutamate Induced Reproductive Behavior Changes in Mice

Mitigation by Aqueous Extract of Celastrus Paniculatus Seeds against Monosodium Glutamate Induced Impairments in Human Neuronal cells IMR-32

The free radicals are considered as primary culprit for many multifactorial diseases. These free radicals scavenging remains a foremost challenge in most neurological disorders, which can be subjected with least collateral damage by herbal extracts. In this study, Celastrus paniculatus (CP) seeds aqueous extract (AE) (0.25, 0.5 and 1.0 µg/ml) was used to evaluate the neuroprotective efficacy against adverse effects of monosodium glutamate (MSG) (7 mM) in neuroblastoma cell line IMR-32. Preliminary pharmacological investigations and free radical scavenging capacity were evaluated for AE. Cytotoxicity and oxidative stress were studied using MTT assay and some biochemical parameters (total protein and glutathione level as well as activity of superoxide dismutase and catalase). Moreover, genotoxicity due to free radicals was also assessed using comet assay in IMR-32 cells. Results showed presence of various phytochemicals in AE and its significant inhibition of DPPH and NO radicals. AE was not only enhancing the activity of antioxidant enzymes but also reduced the free radical mediated cytotoxicity of MSG in IMR-32 cells. The DNA damage found in neuronal cells due to free radical toxicity of MSG was reduced in presence of free radical inhibitory phytochemical present in AE. From these results it can be concluded that AE of CP seeds is an effective antioxidant agent and potent neuroprotective herb to mitigate MSG induced neuronal impairments in IMR-32 cells.

Effect of Embelin in Monosodium Glutamate Induced Obesity in Male Neonatal Wistar Rats

Recent clinical studies report antipsychotics as a better option to augment the action of antidepressants in treatment resistant cases. However, the proper mechanisms underlying the antidepressant effect of antipsychotics is still not clear. Indolamine 2, 3 dioxygenase (IDO) pathway is considered to be an important pathway in pro-inflammatory cytokine associated stress-induced depression. The present study investigated the antidepressant effect of venlafaxine, olanzapine and their combinations in chronic forced-swim stress-induced depression in mice. In addition, the role of pro-inflammatory cytokines and IDO-mediated pathway was investigated. Swiss albino mice were subjected to chronic forced-swim stress and evaluation for antidepressant-like activity was performed on 7th, 14th and 21st day following which serum levels of pro-inflammatory cytokines (IL-1β and IL-6 levels) and the levels of hippocampal kynurenine (KYN), tryptophan (TRP) and serotonin (5HT) were estimated. The combination exhibited augmentation of antidepressant-like activity of venlafaxine by olanzapine in chronic forced-swim stress model. Further, it reversed the enhanced serum IL-1β and IL-6 and reverted the increased activity of IDO as measured by ratio of hippocampal KYN/TRP and 5HT/TRP in stressed mice. Augmentation of antidepressant effect of venlafaxine by olanzapine is thus mediated by normalising the shift from KYN to TRP pathway in chronic forced swim induced stressed mice.

Peripheral CB1 Receptor Neutral Antagonist, AM6545, Ameliorates Hypometabolic Obesity and Improves Adipokine Secretion in Monosodium Glutamate Induced Obese Mice.

Effect of peripheral cannabinoid receptor 1 (CB1R) blockade by AM6545 in the monosodium glutamate (MSG)-induced hypometabolic and hypothalamic obesity was observed, and the impact on intraperitoneal adipose tissue and adipokines was investigated. The MSG mice is characterized by excessive abdominal obesity, and combined with dyslipidemia and insulin resistance. 3-Week AM6545 treatment dose-dependently decreased the body weight, intraperitoneal fat mass, and rectified the accompanied dyslipidemia include elevated serum triglyceride, total cholesterol, free fatty acids, and lowered LDLc level. Glucose intolerance and hyperinsulinemia were also alleviated. But AM6545 didn’t affect the food-intake consistently through the experiment. In line with the reduction on fat mass, the size of adipocyte was reduced markedly. Most interestingly, AM6545 showed significant improvement on levels of circulating adipokines including lowering leptin, asprosin and TNFα, and increasing HMW adiponectin. Correspondingly, dysregulated gene expression of lipogenesis, lipolysis, and adipokines in the adipose tissue were nearly recovered to normal level after AM6545 treatment. Additionally, western blot analysis revealed that AM6545 corrected the elevated CB1R and PPARγ protein expression, while increased the key energy uncoupling protein UCP1 expression in adipose tissue. Taken together, the current study indicates that AM6545 induced a comprehensive metabolic improvement in the MSG mice including counteracting the hypometabolic and hypothalamic obesity, and improving the accompanied dyslipidemia and insulin resistance. One key underlying mechanism is related to ameliorate on the metabolic deregulation of adipose tissue, the synthesis and secretion of adipokines were thus rectified, and finally the catabolism was increased and the anabolism was reduced in intraperitoneal adipose tissue. Findings from this study will provide the valuable information about peripheral CB1R antagonist in managing hypometabolic obesity.

Ameliorative Role of Vitamin D on Prenatal and Postnatal Exposure of Monosodium Glutamate Induced Steatohepatitis in Rat Pups

Background: Monosodium glutamate (MSG) is a widely used flavor enhancer has been linked to obesity and metabolic syndrome, including progressive liver disease. Nonalcoholic Fatty Liver Disease (NAFLD) is the most common hepatic disorder with an etiology related to changes in diet and lifestyle. Prenatal and postnatal exposure to MSG been shown to affect developing tissues in growing animals. Increased Risk of Non-alcoholic Steatohepatitis has been associated with Vitamin D deficiency. The present study was aimed to investigate the ameliorative effect of vitamin D on MSG induced animal models of steatohepatitis in neonatal rats. Materials and Methods: Eighteen nulliparous female wistar rats were randomly divided into three groups (n=6/group). Group-I received a daily oral dose of 5g/kg body weight of MSG. Group-II received the same dose of MSG along with calcitriol (0.2μg/kg BW). Group-III was treated with saline served as the control. The rats could mate, and treatment was given for the entire period of gestation and thirty days thereafter, during lactation. The histological changes in the liver was observed. Results: Pan-lobular microvesicular steatosis, lobular inflammation and ballooning of hepatocytes was observed in the MSG-treated group. These histotoxic changes were ameliorated in the vitamin D treated group. Conclusion: Vitamin D might be beneficial in the protection of the pre-and postnatal exposed MSG induced steatohepatitis. Further, induction of steatohepatitis in a shorter period could also make it an ideal study model of non-alcoholic steatohepatitis.

Monosodium Glutamate Induced Oxidative Stress in Accessory Reproductive Organs of Male Sprague-Dawley Rats

Monosodium Glutamate Induced Oxidative Stress in Accessory Reproductive Organs of Male Sprague-Dawley Rats

Monosodium Glutamate Induced Oxidative Stress in Accessory Reproductive Organs of Male Sprague-Dawley Rats

Monosodium glutamate (MSG) is widely used as a food additive but its excessive intake leads to oxidative stress of several organs. However, the oxidative effect of MSG on male accessory reproductive organs remains unclear. Therefore, the aim of this study was to evaluate the effect of MSG on the status of oxidative stress and morphological alterations in the male accessory reproductive organs such as epididymis, prostate glands and seminal vesicle of Sprague-Dawley rats. A total of 24 male Sprague-Dawley rats were randomly divided into three groups with 8 rats per group. Control group received distilled water (1 ml/kg) while MSG60 and MSG120 received 60 mg/kg and 120 mg/kg of MSG, respectively. All the substances were administered via force feed oral for 28 consecutive days. At the end of the study, the rats were sacrificed to obtain the accessory organs for biochemical analysis and histological observations. The SOD activity in the epididymis showed a significant increase in MSG60 and MSG120 compared to control (p < 0.05). The GSH levels in the epididymis of MSG 120 showed a significant reduction (p <0.05) compared to the control group. The levels of MDA and PC in the epididymis and prostate gland of MSG60 and MSG120 showed a significant increased (p <0.05) compared to the control group. Histological alterations were found in the epididymis and prostate gland of MSG treated rats. In conclusion, MSG at both doses induced oxidative stress in the epididymis and prostate gland of experimental rats. DOI : http://dx.doi.org./10.17576/JSKM-2018-10

Protective Role of Co-administration of Vitamin D in Monosodium Glutamate Induced Obesity in Female Rats

PurposeObesity in females is an emerging health problem. The consumption of MSG has been considered as a risk factor for obesity. The tastemakers in Chinese and fast foods, such as fish sauce and soy sauce, contain very high levels of glutamate. The deficiency of Vitamin D is associated with obesity and metabolic syndrome. Therefore, the present study aimed to determine the effect of co-administration of Vitamin D on body weight control in MSG-induced obese rats. MethodsEighteen adult female Wistar rats were randomly divided into three groups equally. The first group (Group I) was treated with saline served as the control; the second group (Group II) received a daily oral dose of 5 g/kg Body weight of MSG; the third group (Group III) received the same dose of MSG along with calcitriol (0.2 mcg/kg BW) for 15 days. ResultsThe body weight, food, and water intake were measured. MSG treated rats showed a significant increase (P < 0.001) in the body weight, food, and water intake but significant decrease (P < 0.001) was observed in the rats treated with MSG along with Vitamin D. ConclusionIngestion of Vitamin D suppresses body weight gain in MSG-induced obese rats. Active agents in Vitamin D are useful for the prevention and treatment of obesity. Foods tested with high glutamate levels can be fortified with minute quantities of calcitriol to combat the adverse effects without compromising on the taste of the food processed. The fortification of junk foods might also combat largely prevalent Vitamin D deficiency in India.

Study of the Protective Effect of Vitamin C on Monosodium Glutamate Induced Cardiotoxicity in Adult Male Albino Rats

Introduction: Monosodium glutamate (MSG) is worldwide used food flavoring agent. Its safety as food additive is controversial. Vitamin C is a water soluble vitamin with antioxidant activities Aim of the study: The aim of this study was to evaluate the possible toxic effect of MSG on the heart and to evaluate the potential protective effect of concomitant administration of vitamin C together with MSG on the heart of adult male albino rats. Material and methods: The current study was conducted on 60 adult male albino rats. Rats were divided into six equal groups. The first group was used as control group. Group II was treated with vitamin C (100mg/kg/day). Group III was treated with MSG (100mg/kg/day). Group IV was treated with MSG (4g/kg/day). Group V was treated with MSG (100mg/kg/day) together with vitamin C (100mg/kg/day). Group VI was treated with MSG (4g/kg/day) together with vitamin C (100mg/kg/day). All drugs were given orally for 45 days. The weight of the heart was recorded. The level of cardiac troponin I (cTnI) enzyme and the activity of creatine kinase MB (CK- MB) enzyme in serum were assessed. Histopathological examination of heart tissue was carried out. Results: Administration of MSG led to significant increase in the heart weight with significant elevation in the serum cTnI levels and serum CK-MB activity. Sections from low dose MSG treated rats revealed cloudy swelling, while sections form high dose MSG treated rats revealed extensive cloudy swelling with fiber separation and vascular congestion. Concomitant administration of vitamin C together with MSG significantly protected against all these changes Conclusion: It was concluded that MSG is cardiotoxic and that concomitant administration of vitamin C is protective against MSG cardiotoxicity. Recommendations: The current study recommends that the use of MSG should be restricted to very small amounts and should be under supervision of health authorities. The use of vitamin C as a natural and cheap dietary supplement is highly recommended especially in persons who consume diets reach in flavoring agents such as MSG.

Monosodium Glutamate Induced Hepatotoxicity and the Possible Mitigating Effect of Vitamin C and Propolis

Monosodium Glutamate Induced Hepatotoxicity and the Possible Mitigating Effect of Vitamin C and Propolis

Ameliorative Effect of Vitamin C against Monosodium Glutamate Induced Toxicity on Testes and Cauda Epididymal Sperm Reserves in Adult Male Albino Rats

Ameliorative Effect of Vitamin C against Monosodium Glutamate Induced Toxicity on Testes and Cauda Epididymal Sperm Reserves in Adult Male Albino Rats

新生Chinese HamsterにおけるMonosodium Glutamate誘発高血糖症に対する合成Trypsin Inhibitorの効果

新生Chinese HamsterにおけるMonosodium Glutamate誘発高血糖症に対する合成Trypsin Inhibitorの効果

Comparison of Goldthioglucose and Monosodium Glutamateinduced Lesions In the Hypothalamus of Mice

The compound goldthioglucose (GTG) has been shown to produce lesions in the ventromedial region of hypothalamus in mice. Also, lesions in the same region of hypothalamus have been reported after single parenteral administration of monosodium glutamate (MSG). This study has examined the development of these lesions over time with the electron microscope.Mice were given single intraperitoneal injections of either GTG (either 0.2 or 0.6 mg/g body wt) or MSG (either 4.0 or 6.0 mg/g body wt). Animals injected with GTG were killed at times varying between 1 hr - 14 days post injection while those injected with MSG were killed between 3 hours and 3 days after injection. Hypothalamic lesions that developed 3 hours after MSG injection involved only glia cells (Fig. 1) immediately lateral to the base of the third ventricle in the accuate nucleus.