Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity

Hosny, Eman N; Sawie, Hussein G; Elhadidy, Mohamed; Khadrawy, Yasser A.

doi:10.1080/1028415x.2018.1446812

Cited by 32 publications

(17 citation statements)

References 55 publications

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“…The observed morphological lesions in the hepatic and renal tissues of AlCl 3 -intoxicated rats may explain the increased levels of the proinflammatory cytokines TNF- α and IL-1 β as compared with the CON group. The data of the present study agree with the results of Zhang et al [ 40 ], Justin-Thenmozhi et al [ 41 ], and Hosny et al [ 42 ], who found that Al exposure increased the levels of TNF- α and IL-1 β in the liver and kidney tissues of rats.…”

Section: Discussionsupporting

confidence: 93%

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Othman

Fareid

Hameed

et al. 2020

Oxidative Medicine and Cellular Longevity

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Aluminum (Al) is a ubiquitous element with known toxicity for both humans and animals. Herein, we aimed to investigate the potential role of melatonin (MEL) in hepatotoxicity and nephrotoxicity following aluminum chloride (AlCl3) treatment in rats. Adult male rats were treated with AlCl3 (34 mg/kg bwt) for eight weeks. Exposure to AlCl3 enhanced the serum activities of the liver transaminases (alanine aminotransferase and aspartate aminotransferase) and increased the level of bilirubin, in addition to the serum kidney function markers urea and creatinine. AlCl3 intoxication boosted oxidative stress, as evidenced by increases in the levels of lipid peroxidation (LPO) and nitric oxide (NO) along with simultaneous decreases in the levels of glutathione (GSH), various antioxidant enzymes, and Nrf2 mRNA expression. MEL (5 mg/kg bwt) treatment repressed LPO and NO levels, whereas it augmented GSH content. The activities of the antioxidant enzymes GPx, SOD, CAT, and GR were also restored concomitantly when MEL was administered before AlCl3. MEL also suppressed the apoptotic effect of AlCl3 by enhancing Bcl-2 protein expression in the liver and kidney and decreasing the expression levels of proinflammatory cytokines. Histopathological findings in the liver and kidney tissues confirmed the beneficial effect of MEL against AlCl3 toxicity. These findings indicate that MEL prevents AlCl3 toxicity by enhancing the antioxidant defense system.

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Section: Discussionsupporting

confidence: 93%

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Othman

Fareid

Hameed

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Caffeine decreased activity of Na + /K + -ATPase in the cerebral cortex, hippocampus and striatum, and reduced activity of AChE in the cerebral cortex and hippocampus. Also anti-inflammatory properties of caffeine were demonstrated (decreased TNF-α level in the hippocampus and striatum) in AlCl 3 -induced neurotoxicity in rats [143].…”

Section: Non-transgenic Rodent Modelsmentioning

confidence: 89%

“…Generally, experimental studies on caffeine effects in AD demonstrated some beneficial influence on cognition. Its neuroprotective, antioxidant, anti-inflammatory and antiapoptotic activities in the neuronal tissues, led to alleviation of cognitive impairment [104,119,122,123,128,[131][132][133]136,[141][142][143]155,156,158,160,161,[164][165][166]. Many studies pointed out on favorable effects of caffeine on the hallmarks of the disease: Aβ or hyperphosphorylated tau protein [104,117,129,131,134,156,161,162,[164][165][166].…”

Section: Discussionmentioning

confidence: 99%

“…Since AChE inhibitors (donepezil, rivastigmine, galantamine) currently play the main role in the treatment of AD, the effects of caffeine on AChE were also studied. In vivo studies demonstrated weak anticholinesterase activity of caffeine in normal rats [172], in rats with AlCl 3 -induced neurotoxicity [143] and in a nematode AD model [161]. In vitro studies on caffeine and donepezil effects in the rat brain tissue homogenate demonstrated that both drugs inhibited AChE, whereas the effect was stronger after the combined treatment (with stronger inhibition at higher caffeine concentration).…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies showed that caffeine reduced parameters of oxidative stress. Caffeine exerted antioxidant activity in transgenic [104,131] and non-transgenic rodent models [119,123,143], a rabbit model [156], and nematode models [158,161] of AD.…”

Section: Discussionmentioning

confidence: 99%

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Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

et al. 2021

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Alzheimer’s disease (AD) is the most common type of dementia leading to progressive memory loss and cognitive impairment. Considering that pharmacological treatment options for AD are few and not satisfactory, increasing attention is being paid to dietary components that may affect the development of the disease. Such a dietary component may be caffeine contained in coffee, tea or energy drinks. Although epidemiological data suggest that caffeine intake may counteract the development of cognitive impairment, results of those studies are not conclusive. The aim of the present study is to review the existing experimental studies on the efficacy of caffeine against AD and AD-related cognitive impairment, focusing on the proposed protective mechanisms of action. In conclusion, the reports of studies on experimental AD models generally supported the notion that caffeine may exert some beneficial effects in AD. However, further studies are necessary to elucidate the role of caffeine in the effects of its sources on cognition and possibly AD risk.

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High Selenium Yeast mitigates aluminum-induced cerebral inflammation by increasing oxidative stress and blocking NO production

Cao

Qin

et al. 2018

Biometals

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High Selenium Yeast (SeY) serves many important roles with respect to the maintenance of normal nervous system functioning. Studies have reported the nerve inflammation induced by Aluminum (Al) was associated with the increase of mortality. However, in-depth studies are required to verify the hypothesized neuro-protective efficacy of SeY against Al-induced cerebral damage through modulation of the inflammatory response. Here, mice were treated with SeY (0.1 mg/kg) and/or Al (10 mg/kg) by oral gavage for 28 days. Inflammation was assessed by histopathological examination and expression of biomarkers for inflammation. Furthermore, the oxidation-reduction levels and the NO production were assessed using diagnostic kits and RT-PCR. The data indicated that SeY significantly protected cerebrum against Al-induced pathological changes, in addition to the disordered expression of biomarkers of inflammation, the imbalance of oxidation-reduction, and the increase of NO production. Therefore, the chemoprotective potential of SeY against Al-induced cerebral inflammation via restore the levels of oxidation-reduction and the generation of NO was demonstrated.

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Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity

Abstract: The present findings clearly indicate that caffeine provides a significant neuroprotection against AlCl-induced neurotoxicity mediated by its antioxidant, anti-inflammatory, and anticholinesterase properties.

Cited by 32 publications

References 55 publications

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

High Selenium Yeast mitigates aluminum-induced cerebral inflammation by increasing oxidative stress and blocking NO production

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