scholarly journals The Effect of Melatonin on Periodontitis

2021 ◽  
Vol 22 (5) ◽  
pp. 2390
Author(s):  
Barbora Konečná ◽  
Paulína Chobodová ◽  
Jakub Janko ◽  
Lenka Baňasová ◽  
Janka Bábíčková ◽  
...  

Background: Periodontitis is a chronic disease with a complex etiology that includes bacterial colonization, excessive inflammation, and oxidative stress. The hormone melatonin has antioxidant properties and might contribute to alleviating chronic conditions by reducing oxidative stress. The aim of this study was to analyze the effect of exogenous melatonin on periodontitis in an animal model of the disease as well as in patients with periodontitis. Methods: In rats with ligature-induced periodontitis, melatonin was administered in drinking water for two weeks. In the human study, patients with treatment-resistant periodontitis were asked to rinse their mouths with a solution containing melatonin or placebo every evening for two weeks. Periodontal status as well as salivary markers of oxidative stress were assessed at the end of the study. Results: Neither radiography nor μCT revealed any significant effects of melatonin on alveolar bone loss. Gum recession was the only improved macroscopic measure in rats (p < 0.05). Analysis of salivary markers of oxidative stress revealed no effects of treatment in rats or humans despite clearly elevated melatonin concentrations in melatonin treated groups. Conclusion: Our results do not support the use of melatonin for the treatment of periodontitis. However, the negative outcome is limited by the short duration of the study and the chosen route of application as well as the dose of melatonin.

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Naseratun Nessa ◽  
Miyuki Kobara ◽  
Hiroe Toba ◽  
Tetsuya Adachi ◽  
Toshiro Yamamoto ◽  
...  

Introduction: Periodontitis is a lifestyle-related disease that is characterized by chronic inflammation in gingival tissue. Febuxostat, a xanthine oxidase inhibitor, exerts anti-inflammatory and antioxidant effects. Objective: The present study investigated the effects of febuxostat on periodontitis in a rat model. Methods: Male Wistar rats were divided into 3 groups: control, periodontitis, and febuxostat-treated periodontitis groups. Periodontitis was induced by placing a ligature wire around the 2nd maxillary molar and the administration of febuxostat (5 mg/kg/day) was then initiated. After 4 weeks, alveolar bone loss was assessed by micro-computed tomography and methylene blue staining. The expression of osteoprotegerin (OPG), a bone resorption inhibitor, was detected by quantitative RT-PCR and immunological staining, and the number of osteoclasts in gingival tissue was assessed by tartrate-resistant acid phosphatase staining. The mRNA and protein expression levels of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), in gingival tissue were measured using quantitative RT-PCR and immunological staining. Oxidative stress in gingival tissue was evaluated by the expression of 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2-deoxyguanosine (8-OHdG). To clarify the systemic effects of periodontitis, blood pressure and glucose tolerance were examined. Results: In rats with periodontitis, alveolar bone resorption was associated with reductions in OPG and increases in osteoclast numbers. The gingival expression of TNF-α, IL-1β, 4-HNE, and 8-OHdG was up-regulated in rats with periodontitis. Febuxostat significantly reduced alveolar bone loss, proinflammatory cytokine levels, and oxidative stress. It also attenuated periodontitis-induced glucose intolerance and blood pressure elevations. Conclusion: Febuxostat prevented the progression of periodontitis and associated systemic effects by inhibiting proinflammatory mediators and oxidative stress.


Genome ◽  
2011 ◽  
Vol 54 (10) ◽  
pp. 829-835 ◽  
Author(s):  
Mysore S. Ranjini ◽  
Ravikumar Hosamani ◽  
Muralidhara ◽  
Nallur B. Ramachandra

The evolution of karyotypically stabilized short-lived (SL) and long-lived (LL) cytoraces in the laboratory have been established and validated through our previous lifespan studies. In the present investigation, we examined the possible reason(s) for the differential longevity among selected members of SL and LL cytoraces, employing the well known paraquat (PQ) resistance bioassay. Exposure of these races to varying concentrations of PQ revealed relatively higher resistance among LL cytoraces than SL cytoraces, as evident by the lower incidence of mortality. Biochemical analysis for endogenous markers of oxidative stress revealed that LL-2 cytorace exhibited lower reactive oxygen species (ROS) and lipid peroxidation (LPO) levels, higher activity levels of superoxide dismutase (SOD), and coupled with higher levels of reduced glutathione (GSH) compared with the levels found in SL-2 cytorace. These findings suggest that the higher susceptibility of SL cytoraces to PQ challenge may be, at least in part, related to the higher endogenous levels of oxidative stress markers. Although the precise mechanisms responsible for the longer longevity among LL cytoraces of the nasuta–albomicans complex of Drosophila merits further investigation, our data suggest that the relatively longer lifespan may be related to the status of endogenous markers that renders them more resistant towards oxidative-stress-mediated lethality, as evident in the PQ assay.


2021 ◽  
Vol 19 (4) ◽  
pp. 470-476
Author(s):  
Chao Liu ◽  
Chao Liang ◽  
Jie Huang

We have investigated the effect of daphnetin on depressive-like behavior and oxidative stress caused by corticosterone in mice. To this end, we have analyzed the effect of corticosterone alone and combination of corticosterone and daphnetin on three behavioral indices of depressive-like behavior - sucrose consumption rate, forced swimming test, and tail suspension test as well as biochemical markers of oxidative stress - malondialdehyde, nitrite, protein carbonyl, nonprotein sulfhydryl and glutathione contents as well as hippocampal cell apoptosis. The results support the conclusion that daphnetin diminished corticosterone induced depressive like behavior and oxidative stress by activating Nrf2/HO-1 pathway.


2021 ◽  
Vol 99 (Supplement_1) ◽  
pp. 91-92
Author(s):  
Victoria C Wilson ◽  
Brian J Kerr

Abstract The objectives of this study were to determine if feeding thermally processed (TP, heated at 100°C for 120 h) spray-dried egg whites (SDEW) to nursery pigs would impact growth performance, apparent total tract digestibility (ATTD) of GE, N, and S, and oxidative stress. Thirty-two barrows, (initial BW 7.1 kg) were randomly assigned to dietary treatments with 1 pig per pen. In a preliminary study, thermally processing SDEW at 100°C for 120 h increased protein carbonyls (PC) from 6 µmol/g to 19.4 µmol/g (P ≤ 0.01). Diets included either 12% SDEW, 6% TP-SDEW plus 6% SDEW, or 12% TP-SDEW. The experiment lasted 24 d for collection of growth performance data, while plasma was collected on d 21 and liver tissue harvested on d 24 to analyze for markers of oxidative stress. Feces were collected on d 22 for measures of ATTD. Daily gain, daily feed intake, feed efficiency, and ATTD of GE were not found to be different among dietary treatments (P ≥ 0.57). In contrast, ATTD of N (P = 0.11) and S (P = 0.03) were found to increase with increasing protein oxidation in the diet. There was no change in the plasma or liver F2-isoprostanes and 8-hydroxy-2’-deoxyguanosine among dietary treatments (P ≥ 0.28). An increase in plasma PC (P = 0.02) was observed in pigs fed 12% TP-SDEW compared to pigs fed 12% SDEW and pigs fed 6% TP-SDEW. In contrast, a decrease in liver tissue PC (P = 0.04) was observed in pigs fed 6% TP-SDEW compared to pigs fed 12% SDEW and 12% TP-SDEW. These results indicate that feeding TP-SDEW does not affect growth performance, ATTD of GE, and oxidative stress as indicated by F2-isoprostanes or 8-hydroxy-2’-deoxyguanosine; but appeared to have variable effects on oxidative stress as measured by PC.


2021 ◽  
Author(s):  
Zhidong Zhu ◽  
Hui Tang ◽  
Yiqi Zhu ◽  
Hao Wang ◽  
Yanyun Shen

Abstract Background: Systemic sclerosis (SSc) is autoimmune trait affecting several organs, which is identified by thickening of dermis and connective tissue affected by collagen accumulation, as well as vascular injuries inducing hypoxia. Methods: In this investigation, adipose-derived stem cells (ADSCs) were separated from the ADSC exosomes and a bleomycin-induced SSc mouse model was constructed. We employed high-throughput sequencing to study abnormal expression of circular RNAs (circRNAs) in SSc skin tissues with or without ADSC exosome treatment. The regulatory mechanism and targets were studied using bioinformatics analysis, luciferase reporting analysis, angiogenic differentiation experiments, and RT-qPCR detection. Results: ADSC exosome treatment prevented dermal thickening and fibrosis in bleomycin-induced scleroderma. In addition, circ-Zfyve9 was demonstrated to have an important function in ADSC exosome-mediated skin tissue protection. GPX4 and miR-135 were shown to be circ-Zfyve9 downstream targets. Overexpressing miR-135 or downregulating GPX4 reversed circ-Zfyve9 promotion effects rupon angiopoiesis by promoting lipidosome ROS in EPCs under hypoxic conditions. Overexpressing miR-135 or downregulating GPX4 reversed the circ-Zfyve9 inhibition effect on fibrosis in myofibroblasts under hypoxic conditions. Overexpressing circ-Zfyve9 increased the therapeutic effect of ADSC exosomes. Conclusions: Taken together, the present study results show that the exosomes from ADSCs attenuate bleomycin-induced skin fibrosis and oxidative stress in scleroderma via circ-Zfyve9 delivery.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 410-410
Author(s):  
Hyunju Kang ◽  
Young-Ki Park ◽  
Ji-Young Lee

Abstract Objectives Macrophages play an essential role in the development of alcohol-induced inflammation. The objective of this study was to investigate whether nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor naturally found in milk, can attenuate alcohol-induced inflammation and oxidative stress in macrophages with the elucidation of mechanisms of action. Methods RAW 264.7 macrophages and mouse bone marrow-derived macrophages (BMDMs) were stimulated with 80 mM ethanol with or without 1 mM of NR for 72 h. Expression of genes associated with inflammation and oxidative stress and cellular reactive oxygen species (ROS) accumulation were measured. Also, to evaluate the contribution of sirtuin 1 (SIRT1) to the NR's effect, cellular NAD + level (a cofactor of SIRT1), SIRT1 activity, and mitochondrial DNA copy number were measured. SIRT1 activity was inhibited or activated by sirtinol and resveratrol, respectively, to confirm SIRT1 functions further. Parameters related to mitochondrial respiration were determined using a Seahorse XFe24 Extracellular Flux analyzer. Results NR significantly decreased ethanol-induced inflammatory gene expression, with a concomitant decrease in nuclear translocation of nuclear factor kB p65 in macrophages. Increased cellular ROS levels by ethanol were also attenuated concomitantly with decreased expression of NADPH oxidase 2, a ROS-producing enzyme, by NR in both macrophage cell types. Ethanol decreased SIRT1 mRNA, protein and activity, cellular NAD + level, and mitochondrial DNA, all of which were markedly attenuated by NR. SIRT1 inhibition by sirtinol augmented the inflammatory effects of ethanol, while SIRT1 activation by resveratrol elicited the opposing results. Ethanol increased mitochondrial respiration, ATP production, and proton leak, but decreased maximal respiration and spare respiratory capacity. The ethanol-induced changes in mitochondrial respiration were abolished by NR. Conclusions NR showed anti-inflammatory and antioxidant properties in ethanol-treated macrophages by counteracting the effect of ethanol on lowering SIRT1 expression and cellular NAD+ levels. Therefore, NR may be a potential therapeutic agent for alcohol-induced inflammation and oxidative stress. Funding Sources This work is supported by the NIH 3R01DK108254-04S1.


2016 ◽  
Vol 7 (6) ◽  
pp. 2582-2590 ◽  
Author(s):  
Ghada Elmhiri ◽  
Dounia Hamoudi ◽  
Samir Dou ◽  
Narges Bahi-Jaber ◽  
Julie Reygnier ◽  
...  

The present study has been conducted to evaluate the impact of the consumption of high MRP formula on changes in the microbiota and oxidative stress in the colon of IUGR piglets.


2010 ◽  
Vol 104 (9) ◽  
pp. 1357-1362 ◽  
Author(s):  
Helena Petersson ◽  
Ulf Risérus ◽  
Jolene McMonagle ◽  
Hanne L. Gulseth ◽  
Audrey C. Tierney ◽  
...  

Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF2α (a major F2-isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF2α (15-keto-dihydro-PGF2α, a major PGF2α metabolite and marker of cyclooxygenase-mediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α nor those of CRP differed between diet groups at baseline (P>0·07) or at the end of the study (P>0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF2α, P = 0·83; 15-keto-dihydro-PGF2α, P = 0·45; and CRP, P = 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Beatriz Cannizzo ◽  
Agustín Luján ◽  
Natalia Estrella ◽  
Carina Lembo ◽  
Montserrat Cruzado ◽  
...  

High fructose intake induces an insulin resistance state associated with metabolic syndrome (MS). The effect of vascular inflammation in this model is not completely addressed. The aim of this study was to evaluate vascular remodeling, inflammatory and oxidative stress markers, and atheroma development in high-fructose diet-induced insulin resistance of ApoE-deficient mice (ApoE-KO). Mice were fed with either a normal chow or a 10% w/v fructose (HF) in drinking water over a period of 8 weeks. Thereafter, plasma metabolic parameters, vascular remodeling, atheroma lesion size, inflammatory markers, and NAD(P)H oxidase activity in the arteries were determined. HF diet induced a marked increase in plasma glucose, insulin, and triglycerides in ApoE-KO mice, provoked vascular remodeling, enhanced expression of vascular cell-adhesion molecule-1 (VCAM-1) and matrix metalloprotease 9 (MMP-9) and enlarged atherosclerotic lesion in aortic and carotid arteries. NAD(P)H oxidase activity was enhanced by fructose intake, and this effect was attenuated by tempol, a superoxide dismutase mimetic, and losartan, an Angiotensin II receptor antagonist. Our study results show that high-fructose-induced insulin resistance promotes a proinflammatory and prooxidant state which accelerates atherosclerotic plaque formation in ApoE-KO mice.


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