Melatonin reverses type 2 diabetes-induced cognitive deficits via attenuation of oxidative/nitrosative stress and NF-κB-mediated neuroinflammation in rat hippocampus

Zhang, Xuyan; Ping, Ye Jing; Wang, Zhongjing; Sheng, D.; Li, Li; Yang, Fan; Hong, Mao

doi:10.4314/tjpr.v16i12.10

Cited by 5 publications

(2 citation statements)

References 19 publications

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“…30 Moreover, the treatment with melatonin (10 mg/kg) in type 2 diabetic rats for 3 weeks caused a significant decrease in reactive oxygen species (ROS), oxido-nitrosative stress markers, including thiobarbituric acid reactive substances (TBARS), nitrite, and depleted glutathione (GSH) levels in the hippocampus of melatonintreated group. 31 It is suggested that melatonin is one of the most functional scavengers of free radicals. Melatonin acts as a direct scavenger and neutralizes several free radicals such as singlet oxygen, superoxide anion radical, hydroxyl radical, hydroperoxide, lipid peroxide radical, and peroxynitrite.…”

Section: Discussionmentioning

confidence: 99%

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

Javid¹,

Hosseini²,

Gholinezhad³

et al. 2020

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Background and Aim: The imbalance between pro-oxidant and antioxidant systems often leads to further oxidative damage in the pathogenesis of both diabetes and periodontal disease. This study aimed to investigate the antioxidant and anti-inflammatory properties of melatonin in type 2 diabetes mellitus (T2DM) patients with periodontal disease (PD) under non-surgical periodontal therapy (NSPT). Materials and Methods: In this double-blind clinical trial study, 50 T2DM patients with PD were randomly allocated to intervention and control groups and received 250 mg/day (2 tablets) either melatonin or placebo 1 h before bedtime for 8 weeks. The NSPT was performed for all patients in both groups at the beginning of the study. The serum levels of interleukin-1b (IL-1b), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured pre-and post-intervention. Results: Supplementation with melatonin in adjunct to NSPT significantly increased the serum levels of TAC, SOD, CAT, and GPx in the intervention group (P = 0.02, 0.008, 0.004 and 0.004, respectively). The mean changes of SOD, CAT, and GPx were significantly (P = 0.02, 0.04 and 0.04, respectively) greater in the intervention group compared with the control group. Also, after adjusting for confounding factors, the results did not change in terms of significance (P < 0.05). After the intervention, serum levels of MDA and IL-1b were significantly reduced in the intervention group (P < 0.001 and P = 0.008, respectively). The intervention group exhibited lower mean changes of MDA compared with the control group, and these changes were statistically significant (P = 0.008). In addition, after adjusting for confounding factors, the results did not change in terms of significance. Conclusion: The adjunctive effects of melatonin and NSPT may improve inflammatory and antioxidant parameters in T2DM patients with PD.

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Section: Discussionmentioning

confidence: 99%

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

Javid¹,

Hosseini²,

Gholinezhad³

et al. 2020

DMSO

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“…Since the concept of DE was proposed by Nieleson in 1965, our understanding of DE has deepened. Its pathogenesis involves various aspects, including neuroinflammation (2, 3), blood-brain barrier (BBB) (2), vascular factors (4), insulin resistance, insulin deficiency (5, 6), and oxidative stress (3, 6). However, controversy in the literature remains.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR-146a Might Regulate Polarization Transitions of BV-2 Cells Induced by High Glucose and Glucose Fluctuations

et al. 2019

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Microglia are critical in neuroinflammation. M1/M2 polarization transitions of microglial phenotypes determine the states of neuroinflammation and are regulated by multiple pathways, including miRNAs and other epigenetic regulations. This study investigated the polarization transitions of microglia induced by high glucose and glucose fluctuations, and the role of miR-146a in regulating M1/M2 polarization transitions of microglia. BV-2 cells were cultured with 25 mmol/L glucose, 75 mmol/L glucose, and 25 mmol/L−75 mmol/L glucose fluctuation for 48 h. BV-2 cells overexpressing miR-146a were generated using a lentiviral vector. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure mRNA expression of miR-146a, CD11b, iNOS, Arg-1, IRAK1, TRAF6, and NF-κB. Immunofluorescence was used to measure CD11b expression. Western blot was used to measure protein expression of CD11b, iNOS, and Arg-1. Compared with those in the 25 mmol/L glucose control group, expression of CD11b, iNOS, TNF-α, and IL-6 in the 75 mmol/L glucose or glucose fluctuation groups of cultured BV-2 cells were significantly increased, while Arg-1 and IL-10 was significantly decreased. These effects were reversed by overexpression of miR-146a. Furthermore, expression of IRAK1, TRAF6, and NF-κB was significantly increased in the high glucose and glucose fluctuation groups; this was reduced after miR-146a overexpression. In sum, high glucose and glucose fluctuations induced polarization transitions from M1 to M2 phenotype in BV-2 cells. Overexpression of miR-146a might protect BV-2 cells from high glucose and glucose fluctuation associated with M1/M2 polarization transitions by downregulating the expression of IRAK1, TRAF6, and NF-κB.

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Exogenous melatonin restrains neuroinflammation in high fat diet induced diabetic rats through attenuating indoleamine 2,3-dioxygenase 1 expression

et al. 2020

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Melatonin reverses type 2 diabetes-induced cognitive deficits via attenuation of oxidative/nitrosative stress and NF-κB-mediated neuroinflammation in rat hippocampus

Abstract: Purpose: To evaluate the protective effect of melatonin on diabetes-induced cognitive dysfunction. Methods: Rats were fed a high-fat diet + streptozotocin (HFD + STZ) for 15 weeks to induce type 2 diabetes (HFD + STZ group

Cited by 5 publications

References 19 publications

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

<p>Antioxidant and Anti-Inflammatory Properties of Melatonin in Patients with Type 2 Diabetes Mellitus with Periodontal Disease Under Non-Surgical Periodontal Therapy: A Double-Blind, Placebo-Controlled Trial</p>

Overexpression of miR-146a Might Regulate Polarization Transitions of BV-2 Cells Induced by High Glucose and Glucose Fluctuations

Exogenous melatonin restrains neuroinflammation in high fat diet induced diabetic rats through attenuating indoleamine 2,3-dioxygenase 1 expression

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