Melatonin ameliorates cognitive impairment induced by sleep deprivation in rats: Role of oxidative stress, BDNF and CaMKII

Zhang, Lei; Zhang, Huqin; Liang, Xiangyan; Zhang, Haifeng; Zhang, Ting; Liu, Fange

doi:10.1016/j.bbr.2013.07.051

Cited by 111 publications

(94 citation statements)

References 77 publications

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“…These results are corroborated by the previously reported studies indicated that memory deficits are caused by chronic cerebral hypoperfusion [48][49][50][51] . Several previous studies suggested that melatonin [52,53] and resveratrol [54][55][56] treatment alleviates the cognitive deficits in various diseased animal models.…”

Section: Discussionmentioning

confidence: 99%

Effect of Melatonin and Resveratrol against Memory Impairment and Hippocampal Damage in a Rat Model of Vascular Dementia

Shen¹,

Tian²,

Sang³

et al. 2016

Neuroimmunomodulation

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Objectives: This study was intended to investigate whether treatment with resveratrol and melatonin alone or in combination can exert neurorestorative effects in a rat model of vascular dementia. Methods: Briefly, male Wistar rats were subjected to permanent bilateral common carotid artery occlusion (BCCAO) by surgery. After 4 weeks, the cognitive deficits were assessed using the Morris water maze and novel object recognition tests. The biochemical parameters of oxidative stress and inflammation were also assessed. Results: Rats in the BCCAO group showed cognitive deficits, accompanied by oxidonitrosative stress, neuroinflammation, and a reduction in brain-derived neurotrophic factor (BDNF) in the hippocampus region. Moreover, the acetylcholinesterase activity in the hippocampus was found to be increased in the BCCAO group compared to the sham group. The 4-week treatment with melatonin (10 mg/kg) and resveratrol (20 mg/kg) alone and in combination (melatonin 5 mg/kg and reseveratrol 10 mg/kg) caused a significant improvement in the cognitive deficits induced by BCCAO, accompanied by a reversal of oxidonitrosative stress, neuroinflammation, and BDNF depletion in the hippocampus region. Additionally, the treatment with melatonin and resveratrol significantly decreased acetylcholinesterase activity compared to in the BCCAO group. Melatonin and resveratrol ameliorated the BDNF expression of hippocampal protein. Conclusion: These results emphasize that coadministration of melatonin and resveratrol can be beneficial in BCCAO-induced vascular dementia through changes in BDNF expressions.

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Section: Discussionmentioning

confidence: 99%

Effect of Melatonin and Resveratrol against Memory Impairment and Hippocampal Damage in a Rat Model of Vascular Dementia

Shen¹,

Tian²,

Sang³

et al. 2016

Neuroimmunomodulation

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“…The MT does used in this study was chosen on the basis of our previously published experiment. 16 The other groups of rats received the same volume of saline intraperitoneal injection with coordinate content of ethanol at the same time. All experiments were carried out between 8 AM and 5 PM.…”

Section: Study Protocolmentioning

confidence: 99%

“…13,14 The anti-oxidative effect of MT is attributed to both its free radical scavenging activity and the reducing activation of enzymes on the production of reactive oxygen species. 15,16 Moreover, treatment of pharmacologically effective does of MT during the day to rodents, reported to induce sedation, hypothermia and suppression of HPA axis. 17 Enterochromaffin cells of the GI tract are the main source of extra pineal MT and substantially contribute to the peripheral blood concentration of MT.…”

Section: Introductionmentioning

confidence: 99%

Melatonin Attenuates Noise Stress-induced Gastrointestinal Motility Disorder and Gastric Stress Ulcer: Role of Gastrointestinal Hormones and Oxidative Stress in Rats

Zhang

Gong²,

Zhang

et al. 2015

J Neurogastroenterol Motil

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Background/Aims There are increasing evidences for gastrointestinal motility disorder (GIMD) and gastric stress ulcer induced by noise stress. The present study was to investigate the reversed effect of melatonin on GIMD and gastric stress ulcer induced by noise stress and potential mechanism. Methods Noise stress was induced on rats, and melatonin (15 mg/kg) was administered to rats by intraperitoneal injection. Differences were assessed in gastric residual rate (GRR), small intestine propulsion rate (SPR), Guth injury score, cortisol, gastrointestinal hormones (calcitonin-gene-related peptide and motilin) and oxidative stress markers (superoxide dismutase and malondialde hyde) in blood plasma as well as gastric mucosa homogenate with or without melatonin. The pathological examination of gastric mucosa was also performed. Results The GRR and SPR were improved by noise stress compared with control ( P < 0.05). The pathological examination and Guth injury score revealed gastric stress ulcer. Moreover, the levels of cortisol, motilin and malondialdehyde in blood plasma and malondialdehyde in gastric mucosa homogenate were increased by noise stress ( P < 0.05). CGRP and superoxide dismutase activity in both of blood plasma and gastric mucosa homogenate were significantly decreased ( P < 0.05). Furthermore, melatonin reversed changes in GRR, SPR, pathological examination, Guth injury score, cortisol, motilin, CGRP, superoxide dismutase activity and malondialdehyde ( P < 0.05). Conclusions Melatonin is effective in reversing the GIMD and gastric stress ulcer induced by noise stress. The underlying mechanism may be involved in oxidative stress and gastrointestinal hormones.

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“…All these effects allow melatonin to reduce the extent of ROS and improve the oxidative stress-related pathologies as observed in hypertension [67], atherosclerosis [68], cancer [69], ischemia [70], and neurodegenerative diseases [71]. It has also been showed that melatonin ameliorates cognitive impairment induced by sleep deprivation in rats through inhibition of oxidative stress and augmented neurotrophic factors [72].…”

Section: Melatonin: An Antioxidantmentioning

confidence: 98%

Promising Role of Melatonin as Neuroprotectant in Neurodegenerative Pathology

et al. 2014

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Melatonin treatment showed a potent neuroprotective action in experimental models and in clinical studies. However, the entire disease prevention is not observed with melatonin treatment. Therefore, findings have suggested its future use in combination therapies for neurological diseases. Several studies have showed its free radical scavenging, antioxidant property, antiapoptotic activity, and its action towards enhanced mitochondrial function. It has direct and indirect effects on mitochondrial functions. Neurodegenerative disease pathology includes the impaired mitochondrial functions and apoptotic death of neurons due to energy crisis which could be prevented with antiapoptotic activity of melatonin. However, for the therapeutic use of melatonin, researchers also need to pay attention towards the various intermediary events taking place in apoptotic death of neurons during disease pathology. Age-related neurological diseases include the decreased level of melatonin in neuronal death. Therefore, it is worthwhile to discuss about the different functions of melatonin in aspect of its antioxidative property, its role in the enhancement of mitochondrial function, and its antiapoptotic attributes. This review summarizes the reports to date showing the potent role of melatonin in experimental models and clinical trials and discussing the employment of melatonin as future potent neuroprotective agent.

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Melatonin ameliorates cognitive impairment induced by sleep deprivation in rats: Role of oxidative stress, BDNF and CaMKII

Cited by 111 publications

References 77 publications

Effect of Melatonin and Resveratrol against Memory Impairment and Hippocampal Damage in a Rat Model of Vascular Dementia

Effect of Melatonin and Resveratrol against Memory Impairment and Hippocampal Damage in a Rat Model of Vascular Dementia

Melatonin Attenuates Noise Stress-induced Gastrointestinal Motility Disorder and Gastric Stress Ulcer: Role of Gastrointestinal Hormones and Oxidative Stress in Rats

Promising Role of Melatonin as Neuroprotectant in Neurodegenerative Pathology

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