scholarly journals Oral Administration of Resveratrol Alleviates Osteoarthritis Pathology in C57BL/6J Mice Model Induced by a High-Fat Diet

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Mengqi Jiang ◽  
Xingyao Li ◽  
Xiaolu Yu ◽  
Xudan Liu ◽  
Xiaolei Xu ◽  
...  

Obesity has been associated with osteoarthritis (OA) due to increased mass and metabolic factors which are independent of the biomechanical contribution to joint load. Resveratrol, a natural polyphenolic compound, exerts protective effects on OA through its anti-inflammatory property. However, the mechanism of resveratrol on obesity-related OA is unclear. To investigate the effect and possible mechanism of oral resveratrol on obesity-related OA, we fed C57BL/6J mice with a high-fat diet (HFD) for 16 weeks to establish obesity-related OA model; then two doses (22.5 mg/kg and 45 mg/kg) of resveratrol were given by gavage for additional 12 weeks. Mice with HFD significantly increased body weights compared to the control mice, while resveratrol treatment did not cause obvious weight loss. Histological assessments showed that resveratrol at 45 mg/kg significantly improved OA symptoms. Levels of serum IL-1β and leptin were decreased by resveratrol treatment and positively correlated with Mankin scores. Moreover, resveratrol significantly inhibited the expression of TLR4 and TRAF6 in cartilage. These results suggest that HFD induced obesity can lead to the occurrence of OA, and resveratrol may alleviate OA pathology by decreasing the levels of systematic inflammation and/or inhibiting TLR4 signaling pathway in cartilage. Thus, resveratrol might be a promising therapeutic treatment for obesity-related OA.

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1542-1542
Author(s):  
Daphne Weikart ◽  
Vijaya Indukuri ◽  
Kathryn Racine ◽  
Andrew Neilson ◽  
Joshua Lambert

Abstract Objectives Chronic inflammation is an important driver of co-morbidities of obesity. Studies have indicated that cocoa (Theobroma cacao) and cocoa polyphenols can exert anti-inflammatory and anti-obesity properties in animal models. Fermentation and roasting are important for flavor and aroma development of cocoa but have been reported to decrease total phenolic content (TPC).  The effect of these processing steps on anti-inflammatory bioactivity has not been examined in vivo. We examined the impact of fermentation and roasting on the anti-obesity and gastrointestinal protective effects of cocoa in high fat diet (HFD)-fed mice. Methods Male and female mice were fed HFD for 9 wks to induce obesity and then randomized to receive either HFD or HFD supplemented with one of seven cocoa powders (80 mg/g diet) for an additional 8 wks. The cocoa powders differed in terms of roasting (no roast or 30 min at 120°C or 170°C) and fermentation (no, cool, or hot). Body weights were measured weekly. Following euthanasia, serum and cecal digesta were collected. Visceral fat, liver, and spleen were collected and weighed. Small intestine and colon were collected and measured. Prior to euthanasia, gut permeability was measured in a subset of mice from each group. Results Mice treated with cocoa-supplemented diets had lower rate of weight gain: final body weights were 9–13% and 5–19% in males and females, respectively. Cocoa treatment also resulted in longer colon lengths (18–26% in males and 11–24% in females) and reduced gut permeability (50–75% lower) compared to HFD-fed controls indicating reduced colonic inflammation. While fermentation and roasting did impact chemistry and bioactivity, the unfermented, unroasted cocoa was not necessarily the most effective, and some combinations resulted in equivalent or improved bioactivity. Cytokine and microbial composition analysis are ongoing. Conclusions Our results show that all treatments mitigated weight gain, colon inflammation, and gut permeability induced by HFD. The degree of fermentation and roasting and TPC may not predict efficacy. This indicates that it may be possible to develop processing steps to optimize both cocoa flavor and health-related bioactivity. Funding Sources This work was funded by USDA AFRI.


2021 ◽  
Author(s):  
Joe W. E. Moss ◽  
Jessica O Williams ◽  
Wijdan Al-Ahmadi ◽  
Victoria O'Morain ◽  
Yee-Hung Chan ◽  
...  

Atherosclerosis, an inflammatory disorder of the vasculature and the underlying cause of cardiovascular disease, is responsible for one in three global deaths. Consumption of active food ingredients such as omega-3...


PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0201540 ◽  
Author(s):  
Roberta Budriesi ◽  
Fabio Vivarelli ◽  
Donatella Canistro ◽  
Rita Aldini ◽  
Clara Babot Marquillas ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jaime Gonzalez ◽  
Wendy Donoso ◽  
Natalia Díaz ◽  
María Eliana Albornoz ◽  
Ricardo Huilcaman ◽  
...  

Cardiovascular diseases (CVD) represent about 30% of all global deaths. It is currently accepted that, in the atherogenic process, platelets play an important role, contributing to endothelial activation and modulation of the inflammatory phenomenon, promoting the beginning and formation of lesions and their subsequent thrombotic complications. The objective of the present work was to study using immunohistochemistry, the presence of platelets, monocytes/macrophages, and cell adhesion molecules (CD61, CD163, and CD54), in two stages of the atheromatous process. CF-1 mice fed a fat diet were used to obtain early stages of atheromatous process, denominated early stage of atherosclerosis, and ApoE−/−mice fed a fat diet were used to observe advanced stages of atherosclerosis. The CF-1 mice model presented immunostaining on endothelial surface for all three markers studied; the advanced atherosclerosis model in ApoE−/−mice also presented granular immunostaining on lesion thickness, for the same markers. These results suggest that platelets participate in atheromatous process from early stages to advance d stages. High fat diet induces adhesion of platelets to endothelial cellsin vivo. These findings support studying the participation of platelets in the formation of atheromatous plate.


Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3607
Author(s):  
Bojan Stojnić ◽  
Alba Serrano ◽  
Lana Sušak ◽  
Andreu Palou ◽  
M. Luisa Bonet ◽  
...  

Anti-obesity activity has been reported for beta-carotene (BC) supplementation at high doses and metformin (MET). We studied whether BC treatment at a closer to dietary dose and MET treatment at a lower than therapeutic dose are effective in ameliorating unwanted effects of an obesogenic diet and whether their combination is advantageous. Obesity-prone mice were challenged with a high-fat diet (HFD, 45% energy as fat) for 4 weeks while receiving a placebo or being treated orally with BC (3 mg/kg/day), MET (100 mg/kg/day), or their combination (BC+MET); a fifth group received a placebo and was kept on a normal-fat diet (10% energy as fat). HFD-induced increases in body weight gain and inguinal white adipose tissue (WAT) adipocyte size were attenuated maximally or selectively in the BC+MET group, in which a redistribution towards smaller adipocytes was noted. Cumulative energy intake was unaffected, yet results suggested increased systemic energy expenditure and brown adipose tissue activation in the treated groups. Unwanted effects of HFD on glucose control and insulin sensitivity were attenuated in the treated groups, especially BC and BC+MET, in which hepatic lipid content was also decreased. Transcriptional analyses suggested effects on skeletal muscle and WAT metabolism could contribute to better responses to the HFD, especially in the MET and BC+MET groups. The results support the benefits of the BC+MET cotreatment.


2018 ◽  
Vol 315 (6) ◽  
pp. R1085-R1095 ◽  
Author(s):  
Analia S. Loria ◽  
Frank T. Spradley ◽  
Ijeoma E. Obi ◽  
Bryan K. Becker ◽  
Carmen De Miguel ◽  
...  

Clinical studies have shown that obesity negatively impacts large arteries’ function. We reported that rats exposed to maternal separation (MatSep), a model of early life stress, display enhanced angiotensin II (ANG II)-induced vasoconstriction in aortic rings cleaned of perivascular adipose tissue (PVAT) under normal diet (ND) conditions. We hypothesized that exposure to MatSep promotes a greater loss of PVAT-mediated protective effects on vascular function and loss of blood pressure (BP) rhythm in rats fed a high-fat diet (HFD) when compared with controls. MatSep was performed in male Wistar-Kyoto rats from days 2 to 14 of life. Normally reared littermates served as controls. On ND, aortic rings from MatSep rats with PVAT removed showed increased ANG II-mediated vasoconstriction versus controls; however, rings from MatSep rats with intact PVAT displayed blunted constriction. This effect was exacerbated by an HFD in both groups; however, the anticontractile effect of PVAT was greater in MatSep rats. Acetylcholine-induced relaxation was similar in MatSep and control rats fed an ND, regardless of the presence of PVAT. HFD impaired aortic relaxation in rings without PVAT from MatSep rats, whereas the presence of PVAT improved relaxation in both groups. On an HFD, immunolocalization of vascular smooth muscle-derived ANG-(1–7) and PVAT-derived adiponectin abundances were increased in MatSep. In rats fed an HFD, 24-h BP and BP rhythms were similar between groups. In summary, MatSep enhanced the ability of PVAT to blunt the heightened ANG II-induced vasoconstriction and endothelial dysfunction in rats fed an HFD. This protective effect may be mediated via the upregulation of vasoprotective factors within the adipovascular axis.


2021 ◽  
Vol 28 ◽  
Author(s):  
Natália Gonçalves Ribeiro ◽  
Fabio Ribeiro dos Santos ◽  
Janaína Ribeiro Oliveira ◽  
Amanda Souto Machado ◽  
Deborah de Faria Lelis ◽  
...  

Background: Brazilian flora is rich in plants with medicinal properties, which though popular, has contributed to the development of a range of homeopathic products that use plants to treat and cure diseases. However, studies that use Brazilian plants in the treatment of metabolic disorders are still scarce in the literature. Objective: The aim of this study was to analyze the effect of hepatotoxicity Lafoensia pacari on the metabolism of mice with obesity induced by a high-fat diet and to verify the phytochemical difference between the Lafoensia pacari bark of the trunk, leaves, and branches. Methods: The plant material was collected from April to May in the municipality of Bonito de Minas, MG, Brazil. Qualitative tests for the presence of classes of secondary metabolites were performed for leaves, branches and bark of the trunk. Through histological analysis, we evaluated hepatocytes and cell lesions in the liver. Results: The comparative phytochemical analysis of the plant did not reveal alterations between the different plant parts. The phytochemical teste showed that is preferable to use the leaves to make the extract to be applied, aiming to reduce the plant aggression. After treatment, greater changes were observed in the animals that received the high-fat diet and the hydroethanolic extract; the levels of AST, ALT, albumin and creatinine that were increased, thus demonstrating a possible toxicity. There were no significant differences in body weight. In the histological analysis, the animals that received any treatments with the plant, displayed decreased liver weight and reduction in the inflammatory infiltrate. Conclusion: We conclude that Lafoensia pacari should be better evaluated for oral consumption and may cause liver damage.


2019 ◽  
Vol 57 ◽  
pp. 57-65 ◽  
Author(s):  
Merve Acikel Elmas ◽  
Seyit Enes Cakıcı ◽  
Ismail Rahmi Dur ◽  
Ibrahim Kozluca ◽  
Melih Arınc ◽  
...  

Author(s):  
Mao Ouyang ◽  
Tao Qin ◽  
Hengdao Liu ◽  
Junya Lu ◽  
Caixia Peng ◽  
...  

Abstract Objective High-fat diet (HFD) increases the risk of inflammatory reaction and acute arterial thrombosis. Celastrol has been confirmed to regulate inflammatory cytokine levels in atherosclerotic animal models. However, the anti-thrombotic effects of celastrol have remained to be fully demonstrated. The present study was performed to investigate the beneficial effect of celastrol in HFD-induced inflammatory reaction and thrombosis in apolipoprotein (apo)E-/- mice. Materials and Methods Thrombogenic mice model was established using HFD-fed apoE-/- mice. The levels of mRNA and protein were assayed by RT-qPCR and western blotting, respectively. Immunohistochemistry (IHC) staining was performed to measure the protein expression of matrix metalloproteinase-2 and matrix metalloproteinase-9 in the aortic endothelium of HFD-fed apoE-/- mice. Results The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1β signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. In addition, HFD enhanced adenosine diphosphate-induced platelet aggregation in normal C57BL/6 and apoE-/- mice, while celastrol administration reversed this. Furthermore, celastrol inhibited the pro-thrombotic effects of HFD in apoE-/- mice, and the underlying mechanism was mediated, at least partially, through the suppression of matrix metalloproteinase-2 and -9 expression. Conclusions Celastrol administration significantly attenuated HFD-induced inflammatory reaction, platelet aggregation and thrombosis in apoE-/- mice, and celastrol may be used as a drug for the prevention of HFD-induced inflammatory reaction and thrombus.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1353
Author(s):  
Ji Hyun Kim ◽  
Sanghyun Lee ◽  
Eun Ju Cho

Obesity increases risk of Alzheimer’s Disease (AD). A high fat diet (HFD) can lead to amyloidosis and amyloid beta (Aβ) accumulation, which are hallmarks of AD. In this study, protective effects of the ethyl acetate fraction of Acer okamotoanum (EAO) and isoquercitrin were evaluated on obesity and amyloidosis in the HFD- and Aβ-induced mouse model. To induce obesity and AD by HFD and Aβ, mice were provided with HFD for 10 weeks and were intracerebroventricularly injected with Aβ25–35. For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally. Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice. Additionally, EAO- and isoquercitrin-administered groups attenuated abnormal adipokines release via a decrease in leptin and an increase in adiponectin levels compared with the control group. Furthermore, HFD and Aβ-injected mice had damaged liver tissues, but EAO- and isoquercitrin-administered groups attenuated liver damage. Moreover, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice. This study indicated that EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.


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