Neuroprotective effect of green and roasted coffee bean extracts on cerebral ischemia-induced injury in rats

Rizk, Sara; Taha, Heba; Moneim, Ahmed E. Abdel; Amin, Hatem K.

doi:10.1007/s11011-021-00769-6

Cited by 8 publications

(5 citation statements)

References 67 publications

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“…Probably, its antioxidant power depends on the presence of procyanidins and quinic acid derivatives working in synergy. This is in line with a recent study demonstrating that coffee bean extracts reduced the oxidative damage under I/R through the activation of Nrf2 signaling [ 61 ], adding the valuable concept of waste biomass reuse as a source of antioxidant compounds. As the results showed, the different phenolics contained in the Phyt determined specific antioxidant properties able to counteract the oxidative stress generated during the reperfusion, suggesting that the intake of coffee-derived Phyt as a dietary supplement might represent a nutritional strategy to counteract age-related damage.…”

Section: Discussionsupporting

confidence: 89%

Coffee-Derived Phenolic Compounds Activate Nrf2 Antioxidant Pathway in I/R Injury In Vitro Model: A Nutritional Approach Preventing Age Related-Damages

et al. 2022

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Age-related injuries are often connected to alterations in redox homeostasis. The imbalance between free radical oxygen species and endogenous antioxidants defenses could be associated with a growing risk of transient ischemic attack and stroke. In this context, a daily supply of dietary antioxidants could counteract oxidative stress occurring during ischemia/reperfusion injury (I/R), preventing brain damage. Here we investigated the potential antioxidant properties of coffee-derived circulating metabolites and a coffee pulp phytoextract, testing their efficacy as ROS scavengers in an in vitro model of ischemia. Indeed, the coffee fruit is an important source of phenolic compounds, such as chlorogenic acids, present both in the brewed seed and in the discarded pulp. Therefore, rat brain endothelial cells, subjected to oxygen and glucose deprivation (OGD) and recovery (ogR) to mimic reperfusion, were pretreated or not with coffee by-products. The results indicate that, under OGD/ogR, the ROS accumulation was reduced by coffee by-product. Additionally, the coffee extract activated the Nrf2 antioxidant pathway via Erk and Akt kinases phosphorylation, as shown by increased Nrf2 and HO-1 protein levels. The data indicate that the daily intake of coffee by-products as a dietary food supplement represents a potential nutritional strategy to counteract aging.

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Section: Discussionsupporting

confidence: 89%

Coffee-Derived Phenolic Compounds Activate Nrf2 Antioxidant Pathway in I/R Injury In Vitro Model: A Nutritional Approach Preventing Age Related-Damages

et al. 2022

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“…62 Coffee has antiapoptotic effects, which can treat neuronal damage and improve the neurological function caused by ischemic stroke. 63 Recent evidence has revealed that coffee significantly reduceed the levels of Bax and caspase-3, and increases the Bcl-2 level in LPS-induced mice. 64 Moreover, the toxicity of α-syn could be reduced by caffeine, 42 regulating the levels of Bcl-2 and Bax, and then exerting a beneficial effect on dopaminergic neurons.…”

Section: ■ Discussionmentioning

confidence: 99%

“…Studies confirmed that activated Bax induced mitochondrial membrane translocation and released large amounts of Cyt c, leading to increased caspase-3 level as well as neuronal apoptosis. , A growing body of evidence displayed that the decreased levels of Bax and caspase-3 inhibited apoptosis in PD. − Badshah et al revealed that the levels of Bax and caspase-3 were increased in PD rats, accompanied by dyskinesia and an increased number of TH-positive neurons in the substantia nigra compact . Coffee has antiapoptotic effects, which can treat neuronal damage and improve the neurological function caused by ischemic stroke . Recent evidence has revealed that coffee significantly reduceed the levels of Bax and caspase-3, and increases the Bcl-2 level in LPS-induced mice .…”

Section: Discussionmentioning

confidence: 99%

Effect of Coffee against MPTP-Induced Motor Deficits and Neurodegeneration in Mice Via Regulating Gut Microbiota

Liu

Zhang

et al. 2022

J. Agric. Food Chem.

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The mechanisms of coffee against Parkinson disease (PD) remained incompletely elucidated. Numerous studies suggested that gut microbiota played a crucial role in the pathogenesis of PD. Here, we explored the further mechanisms of coffee against PD via regulating gut microbiota. C57BL/6 mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce a PD mouse model, then treated with coffee for 4 consecutive weeks. Behavioral tests consisting of the pole test and beam-walking test were conducted to evaluate the motor function of mice. The levels of tyrosine hydroxylase (TH) and α-synuclein (α-syn) were assessed for dopaminergic neuronal loss. The levels of occludin, glial fibrillary acidic protein (GFAP), Bcl-2, Bax, cleaved caspase-3, and cytochrome c (Cyt c) were detected. Moreover, microbial components were measured by 16s rRNA sequencing. Our results showed that coffee significantly improved the motor deficits and TH neuron loss, and reduced the level of α-syn in the MPTP-induced mice. Moreover, coffee increased the level of BBB tight junction protein occludin and reduced the level of astrocyte activation marker GFAP in the MPTP-induced mice. Furthermore, coffee significantly decreased the levels of proapoptotic proteins, including Bax, cleaved caspase-3, and cytochrome c, while it increased the level of antiapoptotic protein Bcl-2, consequently preventing MPTP-induced apoptotic cascade. Moreover, coffee improved MPTP-induced gut microbiota dysbiosis. These findings suggested that the neuroprotective effects of coffee on PD were involved in the regulation of gut microbiota, which might provide a novel option to elucidate the effects of coffee on PD.

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“…The reaction of both ROS and RNS on cellular biological macromolecules on the biofilm resulted in lipid peroxidation products, such as MDA and 4-hydroxynonenoic acid (4-HNE). According to Rizk et al, 39 nitric oxide reacts with superoxide (O 2 •– ) resulting in the production of peroxynitrite (ONOO •– ), the main cause of NO’s toxic effects. This is also the main cause of tissue injury, following acute nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Nephroprotective Efficacy of Echinops spinosus against a Glycerol-Induced Acute Kidney Injury Model

Rizk,

Abdel Moneim,

Abdel-Gaber

et al. 2023

ACS Omega

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Nephroprotection or renal rescue is to revive and restore kidney function after damage, with no need for further dialysis. During acute kidney injury (AKI), sudden and recent reductions in kidney functions occur. Causes are multiple, and prompt intervention can be critical to diminish or prevent morbidity. Echinops spinosus (ES) is a curative plant with proven pharmacological and biological effects including anti-inflammatory, antioxidant, and antibacterial competencies. The principal goal of this research is to scrutinize the nephroprotective features of E. spinosa extract (ESE) against glycerol-induced AKI. Male Wistar albino rats were equally divided into five separated groups: negative control rats (vehicle-injected), ESE control rats (ESE-treated rats), positive control rats, glycerol-induced AKI-model rats (single IM injection of 50% glycerol), and 2 groups of diseased rats but pretreated with different concentrations of ESE for 7 days (ESE 150 + AKI rats and ESE 250 + AKI rats). Kidney tissues were collected and used for histopathology analysis. The relative kidney weight percentage was assessed. ESE effects were investigated via scanning several biomarkers, such as serum urea and creatinine, as kidney function biomarkers. Lactate dehydrogenase (LDH) and creatine kinase (CK) activities were examined as rhabdomyolysis (RM) indicators. Kidney injury molecule-1 (Kim-1) and neutrophil gelatinase-associated lipocalin (NGAL) were also examined to investigate kidney injury. Enzymatic and nonenzymatic oxidative stress markers were analyzed, namely, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), malondialdehyde (MDA), nitric oxide (NO), and reduced glutathione GSH. Proinflammatory cytokine [tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β)] and the renal proapoptotic protein (Bax) and antiapoptotic protein (Bcl-2) levels were evaluated. Statistical analysis for the resulting data revealed that ESE pretreatment turned AKI-induced biological antioxidant levels to an extent comparable to normal results. Furthermore, ESE decreased kidney function markers and RM-related biomarkers (LDH, CK, Kim-1, and NGAL) compared to those in untreated AKI-model rats. ESE treatment dropped the apoptotic renal Bax levels, enhanced antiapoptotic Bcl-2 manufacture, and disallowed the release of IL-1β and TNF-α. This study revealed the protective effect of ESE as therapeutic medicine against AKI-encouraged oxidative stress, inflammation, and apoptosis. It can be effectively used as adjuvant therapy, helping in renal rescue, and for kidney healing in cases with risk factors of AKI.

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Neuroprotective effect of green and roasted coffee bean extracts on cerebral ischemia-induced injury in rats

Cited by 8 publications

References 67 publications

Coffee-Derived Phenolic Compounds Activate Nrf2 Antioxidant Pathway in I/R Injury In Vitro Model: A Nutritional Approach Preventing Age Related-Damages

Coffee-Derived Phenolic Compounds Activate Nrf2 Antioxidant Pathway in I/R Injury In Vitro Model: A Nutritional Approach Preventing Age Related-Damages

Effect of Coffee against MPTP-Induced Motor Deficits and Neurodegeneration in Mice Via Regulating Gut Microbiota

Nephroprotective Efficacy of Echinops spinosus against a Glycerol-Induced Acute Kidney Injury Model

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