Ginger and turmeric lipid-solubles attenuate heated oil-induced oxidative stress in the brain via the upregulation of NRF2 and improve cognitive function in rats

Zarei, Mahsa; Uppin, Vinayak; Acharya, Pooja; Talahalli, Ramaprasad Ravichandra

doi:10.1007/s11011-020-00642-y

Cited by 12 publications

(6 citation statements)

References 46 publications

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“…Our study is the first study to prove that the beneficial synergetic effect of cinnamon and ginger oils on oxidative stress in the prefrontal cortex, which was chronically exposed to nicotine, may be due to the combined its polyphenols content. This is consistent with [39] who confirmed the beneficial antioxidant effect of ginger separately and also with [40] who studied the antioxidant effect of ginger on acetaminophen overdose, but in our study, we found that the combination of cinnamon and ginger has significant improvement in oxidative stress markers, compared to cinnamon and ginger when used separately.…”

Section: Discussionsupporting

confidence: 93%

Ameliorating Effect of Combined Cinnamon and Ginger Oils against the Neurotoxicity of Nicotine Administration on the Prefrontal Cortex of Adult Albino Rats: Immunohistochemical and Ultrastructural Study

et al. 2021

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Background: Nicotine is the active alkaloid in cigarettes. It was reported that tobacco smoking has many hazards; one of these hazards is the effect on the cognitive function of the prefrontal cortex. The aim of our study is to investigate the antioxidant effects of ginger, cinnamon oils, and their combination on morphological changes in the prefrontal cortex that were induced by nicotine. Materials and methods: Fifty adult male albino rats were divided into five groups: group I (control group), group II (nicotine), group III (nicotine + cinnamon), group IV (nicotine + ginger), and group V (nicotine + cinnamon + ginger). The coronal sections from the anterior part of the rat brain at the site of prefrontal cortex were examined by light microscope for (H&E and immunohistochemical staining with TNF-α and GFAP), while the ultrastructure morphology was examined by transmission electron microscopy. Levels of the oxidative stress markers (MDA, GSH) in the rats’ brain tissue homogenate were biochemically assessed. Results: Compared to the control group, the rats that were treated with nicotine (group II) showed a significant oxidative stress in the form of marked elevation of MDA and decrease in GSH, apoptotic changes especially in the pyramidal cells in the form of neuronal cell degeneration and pyknosis, and an elevation in the inflammatory marker TNF-α and GFAP expressions. These changes were observed to a lesser degree in rat group (III) and group (IV), while there was a marked improvement achieved by the combined usage of cinnamon and ginger oils, together compared to the nicotine group. Conclusions: Ginger and cinnamon are powerful antioxidants which ameliorate the degenerative and oxidative effects produced by nicotine on a rat’s prefrontal cortex.

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Section: Discussionsupporting

confidence: 93%

Ameliorating Effect of Combined Cinnamon and Ginger Oils against the Neurotoxicity of Nicotine Administration on the Prefrontal Cortex of Adult Albino Rats: Immunohistochemical and Ultrastructural Study

et al. 2021

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“…HFD increases oxidative stress by lowering the level of antioxidant enzymes in brain 5 . Due to oxidative stress, SOD, which initiate the cellular defense system, changes the superoxide anion into H 2 O 2 , simultaneously others defensive enzymes i.e.…”

Section: Discussionmentioning

confidence: 99%

“…The consumption of HFD for the long term deregulates the normal functioning of various organs, including brain. Many evidences depict that it impairs the cognitive function and elevates the susceptibility to anxiety 3 , 4 by formation of reactive oxygen species (ROS) and causes the oxidative stress and weakens the antioxidant mechanism in the brain 5 . However, the harmful effects of obesity in brain are still not clear, but previous findings had suggested that body fat deposition and obesity play an essential role in certain brain-associated disorders 6 , 7 such as memory and learning dysfunction in the humans 8 and in animal models 9 and showed anxiety like behavior 10 due to alteration in the levels of neurotransmitters and hormones which cause behavioral deficits 11 .…”

Section: Introductionmentioning

confidence: 99%

Protective effects of niacin following high fat rich diet: an in-vivo and in-silico study

Samad,

Manzoor,

Batool

et al. 2023

Sci Rep

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Niacin had long been understood as an antioxidant. There were reports that high fat diet (HFD) may cause psychological and physical impairments. The present study was aimed to experience the effect of Niacin on % growth rate, cumulative food intake, motor activity and anxiety profile, redox status, 5-HT metabolism and brain histopathology in rats. Rats were administered with Niacin at a dose of 50 mg/ml/kg body weight for 4 weeks following normal diet (ND) and HFD. Behavioral tests were performed after 4 weeks. Animals were sacrificed to collect brain samples. Biochemical, neurochemical and histopathological studies were performed. HFD increased food intake and body weight. The exploratory activity was reduced and anxiety like behavior was observed in HFD treated animals. Activity of antioxidant enzymes was decreased while oxidative stress marker and serotonin metabolism in the brain of rat were increased in HFD treated animals than ND fed rats. Morphology of the brain was also altered by HFD administration. Conversely, Niacin treated animals decreased food intake and % growth rate, increased exploratory activity, produced anxiolytic effects, decreased oxidative stress and increased antioxidant enzyme and 5-HT levels following HFD. Morphology of brain is also normalized by the treatment of Niacin following HFD. In-silico studies showed that Niacin has a potential binding affinity with degradative enzyme of 5-HT i.e. monoamine oxidase (MAO) A and B with an energy of ~ − 4.5 and − 5.0 kcal/mol respectively. In conclusion, the present study showed that Niacin enhanced motor activity, produced anxiolytic effect, and reduced oxidative stress, appetite, growth rate, increased antioxidant enzymes and normalized serotonin system and brain morphology following HFD intake. In-silico studies suggested that increase 5-HT was associated with the binding of MAO with Niacin subsequentially an inhibition of the degradation of monoamine. It is suggested that Niacin has a great antioxidant potential and could be a good therapy for the treatment of HFD induced obesity.

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“…Our findings suggested dietary peroxides may not be a significant source of lipid peroxides in the circulation, as they can be reduced to corresponding hydroxides during the digestion process. Some in vivo studies demonstrated oxidative stress was induced by consuming heated oils, potentially due to the secondary effects of lipid peroxide-derived products rather than the original compounds (e.g., [ 69 ]). We have demonstrated here, however, that 13-HPODE decreases PON1 activity, potentially preventing a source of significant antioxidant activity.…”

Section: Discussionmentioning

confidence: 99%

Intestinal and Hepatic Uptake of Dietary Peroxidized Lipids and Their Decomposition Products, and Their Subsequent Effects on Apolipoprotein A1 and Paraoxonase1

et al. 2021

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Both pro- and antiatherosclerotic effects have been ascribed to dietary peroxidized lipids. Confusion on the role of peroxidized lipids in atherosclerotic cardiovascular disease is punctuated by a lack of understanding regarding the metabolic fate and potential physiological effects of dietary peroxidized lipids and their decomposition products. This study sought to determine the metabolic fate and physiological ramifications of 13-hydroperoxyoctadecadienoic acid (13-HPODE) and 13-HODE (13-hydroxyoctadecadienoic acid) supplementation in intestinal and hepatic cell lines, as well as any effects resulting from 13-HPODE or 13-HODE degradation products. In the presence of Caco-2 cells, 13-HPODE was rapidly reduced to 13-HODE. Upon entering the cell, 13-HODE appears to undergo decomposition, followed by esterification. Moreover, 13-HPODE undergoes autodecomposition to produce aldehydes such as 9-oxononanoic acid (9-ONA). Results indicate that 9-ONA was oxidized to azelaic acid (AzA) rapidly in cell culture media, but AzA was poorly absorbed by intestinal cells and remained detectable in cell culture media for up to 18 h. An increased apolipoprotein A1 (ApoA1) secretion was observed in Caco-2 cells in the presence of 13-HPODE, 9-ONA, and AzA, whereas such induction was not observed in HepG2 cells. However, 13-HPODE treatments suppressed paraoxonase 1 (PON1) activity, suggesting the induction of ApoA1 secretion by 13-HPODE may not represent functional high-density lipoprotein (HDL) capable of reducing oxidative stress. Alternatively, AzA induced both ApoA1 secretion and PON1 activity while suppressing ApoB secretion in differentiated Caco-2 cells but not in HepG2. These results suggest oxidation of 9-ONA to AzA might be an important phenomenon, resulting in the accumulation of potentially beneficial dietary peroxidized lipid-derived aldehydes.

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Ginger and turmeric lipid-solubles attenuate heated oil-induced oxidative stress in the brain via the upregulation of NRF2 and improve cognitive function in rats

Cited by 12 publications

References 46 publications

Ameliorating Effect of Combined Cinnamon and Ginger Oils against the Neurotoxicity of Nicotine Administration on the Prefrontal Cortex of Adult Albino Rats: Immunohistochemical and Ultrastructural Study

Ameliorating Effect of Combined Cinnamon and Ginger Oils against the Neurotoxicity of Nicotine Administration on the Prefrontal Cortex of Adult Albino Rats: Immunohistochemical and Ultrastructural Study

Protective effects of niacin following high fat rich diet: an in-vivo and in-silico study

Intestinal and Hepatic Uptake of Dietary Peroxidized Lipids and Their Decomposition Products, and Their Subsequent Effects on Apolipoprotein A1 and Paraoxonase1

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