Metabolic Alterations and the Protective Effect of Punicalagin Against Glutamate-Induced Oxidative Toxicity in HT22 Cells

Pathakoti, Kavitha; Goodla, Lavanya; Manubolu, Manjunath; Tencomnao, Tewin

doi:10.1007/s12640-016-9697-2

Cited by 25 publications

(15 citation statements)

References 55 publications

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“…Unlikely, Ran which reduced these alterations without normalization indicating the superior antioxidant property of PCG to the standard drug; Ran. Previous studies also displayed the antioxidant property of PCG [11,12,[23][24][25].…”

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confidence: 84%

Gastroprotective Effect of Punicalagin against Ethanol-Induced Gastric Ulcer: The Possible Underlying Mechanisms

Mohamed¹,

Salahuddin²

2017

Biomark J

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Gastric ulcer is the most digestive disease found in clinical practice. Punicalagin (PCG) found in pomegranate juice has antioxidant and tissue repair properties. Therefore, the aim of this study was to investigate punicalagin's gastroprotective effect against ethanol-induce gastric injury. Four groups of rats; first group served as control, group 2: Treated with absolute ethanol (5 ml/kg, po), group 3: Rats were pre-treated with ranitidine (as a reference drug) (50 mg/kg, po) before ethanol and group 4: Pre-treated with PCG (4 mg/kg, po) before ethanol. Pretreatment with PCG reduced ulcer index and histopathological changes, oxidative stress induced by ethanol while it elevated antioxidant activity. Although, it down regulated Tumor Necrosis Factor (TNF-α) gene expression and mucosal levels of inflammatory cytokines; TNF-α, Interleukin (IL-1β) and Interferon Gamma (IFNγ), it up regulated mucosal level of IL-10. Also, it reduced mucosal Nuclear Factor Kappa B (NFκB) protein expression, mylopeoxidase and caspase 3 activities as well as gene expression of caspase 9 while it elevated antiapoptotic B-Cell Lymphoma 2 (Bcl-2) gene expression, mucosal nitric oxide and mucin content. However, it had negative action on prostaglandin E2 and acid secretions. These findings indicate gastroprotective effects of punicalagin against ethanol induced gastric ulcer through suppression of mucosal oxidative stress and inflammation through NFκB pathway as well cytoprotective defences independent on prostaglandin E2 and acid secretions.

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confidence: 84%

Gastroprotective Effect of Punicalagin against Ethanol-Induced Gastric Ulcer: The Possible Underlying Mechanisms

Mohamed¹,

Salahuddin²

2017

Biomark J

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“…Oxidative stress promotes neurotoxicity by increasing amyloid beta (A β ) aggregation concomitantly with inflammatory events such as reactive oxygen species (ROS) production [ 3 ]. Additionally, excess extracellular glutamate levels have been found to correlate with the development of neurodegenerative disorders by triggering oxidative glutamate damage, preventing the intracellular antioxidant synthesis, and ultimately leading to ROS accumulation [ 4 ]. The overproduction of ROS and A β causes a feedback loop that results in synaptic dysfunction, as well as mitochondria-mediated apoptosis [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Basis for Use of Armillaria mellea Polysaccharides in Alzheimer’s Disease: Antiapoptosis and Antioxidation

Lü

Zhang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Armillaria mellea, an edible fungus, exhibits various pharmacological activities, including antioxidant and antiapoptotic properties. However, the effects of A. mellea on Alzheimer's disease (AD) have not been systemically reported. The present study aimed to explore the protective effects of mycelium polysaccharides (AMPS) obtained from A. mellea, especially AMPSc via 70% ethanol precipitation in a L-glutamic acid- (L-Glu-) induced HT22 cell apoptosis model and an AlCl3 plus D-galactose- (D-gal-) induced AD mouse model. AMPSc significantly enhanced cell viability, suppressed nuclear apoptosis, inhibited intracellular reactive oxygen species accumulation, prevented caspase-3 activation, and restored mitochondrial membrane potential (MMP). In AD mice, AMPSc enhanced horizontal movements in an autonomic activity test, improved endurance times in a rotarod test, and decreased escape latency time in a water maze test. Furthermore, AMPSc reduced the apoptosis rate, amyloid beta (Aβ) deposition, oxidative damage, and p-Tau aggregations in the AD mouse hippocampus. The central cholinergic system functions in AD mice improved after a 4-week course of AMPSc administration, as indicated by enhanced acetylcholine (Ach) and choline acetyltransferase (ChAT) concentrations, and reduced acetylcholine esterase (AchE) levels in serum and hypothalamus. Our findings provide experimental evidence suggesting A. mellea as a neuroprotective candidate for treating or preventing neurodegenerative diseases.

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“…This disturbs the membrane integrity and Ca 2+ homeostasis to produce hepatocellular damage [36]. The use of phytochemicals with antioxidant activity can offer protection against the oxidative damage [37]. The present investigation revealed that an ethanolic extract of A. baccifera (EEAB) significantly attenuated the CCl 4 induced oxidative stress by augmenting the endogenous antioxidant levels.…”

Section: Discussionmentioning

confidence: 69%

Protective Effects of Ammannia baccifera Against CCl4-Induced Oxidative Stress in Rats

Goodla

Manubolu

Pathakoti

et al. 2019

IJERPH

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Ammannia baccifera Linn. is commonly used as a traditional medicine in India and China. The antioxidant potential of an ethanolic extract of A. baccifera (EEAB; 250 mg/kg and 500 mg/kg) was evaluated against CCL4-induced toxicity in rats. Antioxidant activity was assessed by measuring the enzymatic and non-enzymatic antioxidants. Phytochemical constituents of EEAB were also analyzed by using UHPLC-QTOF-MS. EEAB treatment markedly reduced CCl4 effects on lipid peroxidation, cholesterol, triacylglycerides, and protein carbonyls. It increased the levels of phospholipids, total sulfhydryl, and antioxidant enzymes, which were reduced by CCl4 intoxication. Treatment with EEAB significantly alleviated the CCl4 effect on non-enzymatic antioxidants. Isoenzyme pattern analyses revealed that significant alterations in superoxide dismutase (SOD1), glutathione peroxidase (GPx2, GPx3), and catalase (CAT) occurred in rats that were exposed to CCl4 and restored post EEAB treatment. Moreover, CCl4-induced down regulation of SOD, CAT, and GPx gene expression was conversely counteracted by EEAB. Its bioactivity may be due to its incorporation of major compounds, such as chlorogenic acid, quercetin, protocatechuic acid, lamioside, crocetin, and khayasin C. These results suggest that EEAB may be used as a potent antioxidant and hepatoprotective agent since it is a rich source of flavonoids and phenolic compounds.

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Metabolic Alterations and the Protective Effect of Punicalagin Against Glutamate-Induced Oxidative Toxicity in HT22 Cells

Cited by 25 publications

References 55 publications

Gastroprotective Effect of Punicalagin against Ethanol-Induced Gastric Ulcer: The Possible Underlying Mechanisms

Gastroprotective Effect of Punicalagin against Ethanol-Induced Gastric Ulcer: The Possible Underlying Mechanisms

Pharmacological Basis for Use of Armillaria mellea Polysaccharides in Alzheimer’s Disease: Antiapoptosis and Antioxidation

Protective Effects of Ammannia baccifera Against CCl4-Induced Oxidative Stress in Rats

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