L-carnitine and Co Q10 ameliorate potassium dichromate -induced acute brain injury in rats targeting AMPK/AKT/NF-κβ

Salama, Abeer; Elgohary, Rania

doi:10.1016/j.intimp.2021.107867

Cited by 17 publications

(15 citation statements)

References 48 publications

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“…And it was reported that maternal HF feeding reduced the level of free-carnitine, short-chain and medium-chain acylcarnitines in the placenta ( 42 ), and decreased the level of L-carinitine in the liver of offspring ( 43 ). Oral L-carnitine administration can increase AMPK protein expression ( 44 , 45 ). Thus, we supposed that maternal HF feeding may affect the FAO in the offspring through imbalanced carnitine.…”

Section: Resultsmentioning

confidence: 99%

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Zhang

Wang

et al. 2022

Front. Nutr.

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Maternal overnutrition can affect fetal growth and development, thus increasing susceptibility to obesity and diabetes in later life of the offspring. Placenta is the central organ connecting the developing fetus with the maternal environment. It is indicated placental fatty acid metabolism plays an essential role in affecting the outcome of the pregnancy and fetus. However, the role of placental fatty acid β-oxidation (FAO) in maternal overnutrition affecting glucose metabolism in the offspring remains unclear. In this study, C57BL/6J female mice were fed with normal chow or high-fat diet before and during pregnancy and lactation. The placenta and fetal liver were collected at gestation day 18.5, and the offspring's liver was collected at weaning. FAO-related genes and AMP-activated protein kinase (AMPK) signaling pathway were examined both in the placenta and in the human JEG-3 trophoblast cells. FAO-related genes were further examined in the liver of the fetuses and in the offspring at weaning. We found that dams fed with high-fat diet showed higher fasting blood glucose, impaired glucose tolerance at gestation day 14.5 and higher serum total cholesterol (T-CHO) at gestation day 18.5. The placental weight and lipid deposition were significantly increased in maternal high-fat diet group. At weaning, the offspring mice of high-fat diet group exhibited higher body weight, impaired glucose tolerance, insulin resistance and increased serum T-CHO, compared with control group. We further found that maternal high-fat diet downregulated mRNA and protein expressions of carnitine palmitoyltransferase 2 (CPT2), a key enzyme in FAO, by suppressing the AMPK/Sirt1/PGC1α signaling pathway in the placenta. In JEG-3 cells, protein expressions of CPT2 and CPT1b were both downregulated by suppressing the AMPK/Sirt1/PGC1α signaling pathway under glucolipotoxic condition, but were later restored by the AMPK agonist 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR). However, there was no difference in CPT2 and CPT1 gene expression in the liver of fetuses and offspring at weaning age. In conclusion, maternal high-fat diet can impair gene expression involved in FAO in the placenta by downregulating the AMPK signaling pathway, and can cause glucose and lipid dysfunction of offspring at weaning, indicating that placental FAO may play a crucial role in regulating maternal overnutrition and metabolic health in the offspring.

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Section: Resultsmentioning

confidence: 99%

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Zhang

Wang

et al. 2022

Front. Nutr.

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“…This observation was consistent with the observations of Chakraborty et al (2022) on chromium toxicity in the lung, liver, and kidney. Salama & Elgohary (2021) attributed it to the inflammatory effects of potassium dichromate.…”

Section: Discussionmentioning

confidence: 99%

“…It is reduced in the body by substances like glutathione and ascorbate, providing an unstable pentavalent and a stable trivalent chromium (Ray, 2016). During the process of reduction, reactive oxygen species (ROS) are produced (Salama and Elgohary, 2021).…”

Section: Introductionmentioning

confidence: 99%

Possible Protective Role of Nanoselenium against Potassium Dichromate-Induced Splenic Toxicity in Adult Male Albino Rat: Histological, Histochemical, Immunohistochemical and Morphometric Study

Bushra

Shenouda²

2022

Egyptian Academic Journal of Biological Sciences, D. Histology

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Introduction:The spleen is a large lymphoid organ that plays an important role in immunity. Potassium dichromium is well-known to be toxic. Nanoselenium is a potent antioxidant trace mineral. The aim of the work was to explore the influence of potassium dichromate on the spleen and the co-administration of nanoselenium against the induced splenic injury. Material and methods: 30 adult male albino rats (200-250g) were equally randomly divided into three groups. Group I (the control group) received no treatment. Group II (the chromium-treated group) received potassium dichromate (2 mg/kg b.w. dispersed in 1 ml distilled water) intraperitoneally daily for 2 weeks. Group III (the chromium and selenium-treated group) received nanoselenium (0.5 mg/kg b.w. dissolved in 0.5 ml of phosphate-buffered saline, intraperitoneally) as well as potassium dichromate (2 mg/kg b.w. dispersed in 1 ml distilled water) intraperitoneally daily for 2 weeks. Then, the spleens of all groups were extracted and processed to be studied. Results: The chromiumtreated group revealed disturbance of the architecture of the white pulp, congestion of the red pulp, deposition of hemosiderin pigments, chromatin condensation of the lymphocytes' nuclei, and markedly dilated rough endoplasmic reticulum of the plasma cells. There were significant increases in the area percentage of collagen fibers deposition and iron staining and a significant decrease in the area percentage of Bcl-2 immune expression. The administration of nanoselenium in Group III ameliorated most of these toxic effects. Conclusion: Nanoselenium exhibited a protective role against the toxic effect of potassium dichromate on the spleen.

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“…Histopathological examination for the brain tissues of the control and treated groups were performed. Brain tissues were fixed in 10% formalin and processed for paraffin sections of 4 μm thick, then stained by hematoxylin and eosin (H&E) [39]. The number of intact pyramidal neurons per 1 mm of the hippocampus is quantified at 400 magnifications.…”

Section: Histopathological Examinationmentioning

confidence: 99%

Influence of chrysin on D‐galactose induced‐aging in mice: Up regulation of AMP kinase/liver kinase B1/peroxisome proliferator‐activated receptor‐γ coactivator 1‐α signaling pathway

Salama

Elgohary

2023

Fundamemntal Clinical Pharma

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Adenosine monophosphate kinase/liver kinase B1/peroxisome proliferator‐activated receptor‐γ coactivator 1‐α (AMPK/LKB1/PGC1α) pathway has a vital role in regulating age‐related diseases. It controls neurogenesis, cell proliferation, axon outgrowth, and cellular energy homeostasis. AMPK pathway also regulates mitochondrial synthesis. The current study evaluated the effect of chrysin on D‐galactose (D‐gal) induced‐aging, neuron degeneration, mitochondrial dysfunction, oxidative stress, and neuroinflammation in mice. The mice were allocated randomly into four groups (10 each group): Group 1: normal control group, Group 2: D‐gal group, Groups 3 and 4: chrysin (125 and 250 mg/kg, respectively). Groups 2–4 were injected with D‐gal (200 mg/kg/day; s.c) for 8 weeks to induce aging. Groups 3 and 4 were orally gavaged every day concurrent with D‐gal. At the end of experiment, behavioral, brain biochemical and histopathological changes were monitored. Chrysin administration elevated discrimination ratio in object recognition, Y Maze percentage alternation, locomotor activity and brain contents of AMPK, LKB1, PGC1α, NAD (P)H quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HO‐1), nerve growth factor (NGF) (neurotrophin‐3; NT‐3), and seretonin as well as reduced brain contents of tumor necrosis factor‐alpha (TNF‐α), nuclear factor kappa B (NF‐κB), advanced glycation end products (AGEs) and glial fibrillary acidic protein (GFAP) compared to D‐gal‐treated mice. Chrysin also alleviated cerebral cortex and white matter neurons degeneration. Chrysin protects against neurodegeneration, improves mitochondrial autophagy and biogenesis as well as activates antioxidant genes expression. In addition, chrysin ameliorates neuroinflammation and stimulates the release of NGF and serotonin neurotransmitter. So, chrysin has a neuroprotective effect in D‐gal induced‐aging in mice.

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L-carnitine and Co Q10 ameliorate potassium dichromate -induced acute brain injury in rats targeting AMPK/AKT/NF-κβ

Cited by 17 publications

References 48 publications

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Maternal High-Fat Diet Impairs Placental Fatty Acid β-Oxidation and Metabolic Homeostasis in the Offspring

Possible Protective Role of Nanoselenium against Potassium Dichromate-Induced Splenic Toxicity in Adult Male Albino Rat: Histological, Histochemical, Immunohistochemical and Morphometric Study

Influence of chrysin on D‐galactose induced‐aging in mice: Up regulation of AMP kinase/liver kinase B1/peroxisome proliferator‐activated receptor‐γ coactivator 1‐α signaling pathway

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