scholarly journals Curcumin Inhibits Age-Related Vascular Changes in Aged Mice Fed a High-Fat Diet

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1476 ◽  
Author(s):  
Kenichiro Takano ◽  
Junko Tatebe ◽  
Naohiro Washizawa ◽  
Toshisuke Morita
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Heme Oxygenase 1 ◽  
Vascular Aging ◽  
High Fat ◽  
Sirt1 Expression ◽  
Age Related ◽  
Westernized Diet ◽  
Term Administration ◽  
Oxidative Effects

Inhibiting the onset of arteriosclerotic disease, which has been increasing due to the westernized diet and aging, is a significant social challenge. Curcumin, a type of polyphenol, has anti-oxidative effects and anti-inflammatory action and is expected to treat and to have prophylactic effects on different diseases. In this study, we examined the effects of long-term administration of curcumin on vascular aging and chronic inflammation—the causes of arteriosclerotic disease. Eight-week-old C57BL/6J mice were fed with high fat diet (HFD) or 0.1% curcumin-mixed HFD (HFD + Cu) until 80 weeks old (n = 20 for each group). After the breeding, we examined the expression of antioxidant enzymes, heme oxygenase-1 (HO-1), oxidative stress, vascular aging, and inflammatory changes in the aorta. In the HFD group, oxidative stress increased with decreased sirt1 expression in the aorta followed by increased senescent cells and enhanced inflammation. Whereas in the HFD + Cu group, HO-1 was induced in the aorta with the suppression of oxidative stress. Additionally, it was shown that sirt1 expression in the aorta in the HFD + Cu group remained at a level comparable to that of the 8-week-old mice with suppression of increased senescent cells and enhanced inflammation. Consequently, disorders associated with HFD were resolved. These results suggest that curcumin might be a food with a prophylactic function against arteriosclerotic disease.

Effect of curcumin on hepatic heme oxygenase 1 expression in high fat diet fed rats: is there a triangular relationship?

2014 ◽  
Vol 92 (10) ◽  
pp. 805-812 ◽  
Author(s):  
Yıldız Öner-İyidoğan ◽  
Sevda Tanrıkulu-Küçük ◽  
Muhammed Seyithanoğlu ◽  
Hikmet Koçak ◽  
Semra Doğru-Abbasoğlu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Liver ◽  
Heme Oxygenase ◽  
High Fat Diet ◽  
Control Diet ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Curcumin Treatment ◽  
Fat Accumulation ◽  
Hepatic Fat

High fat diet (HFD) is associated with oxidative stress induced fatty liver. Curcumin, an extract of Curcuma longa, has been shown to possess potent antioxidant and hypolipidemic properties. In this study, we investigated the effect of curcumin treatment on hepatic heme oxygenase-1 (HO-1) expression along with pro-oxidant–antioxidant status and lipid accumulation in rats fed an HFD. Male Sprague–Dawley rats were distributed among 4 groups: Group 1, which was fed the control diet (10% of total calories from fat); Group 2, which was fed the HFD (60% of total calories from fat); and groups 3 and 4, which received the HFD supplemented with curcumin and the control diet supplemented with curcumin (1 g/kg diet; w/w), respectively, for 16 weeks. HFD caused increases in hepatic lipid levels, production of reactive oxygen species, and lipid peroxidation. Further, HO-1 expression was significantly decreased. Histopathological examination showed hepatic fat accumulation and slight fibrotic changes. Curcumin treatment reduced hepatic lipids and oxidative stress parameters, and HO-1 expression was significantly increased. These findings suggest that increased HO-1 expression, along with suppressed oxidative stress as well as reduced hepatic fat accumulation and fibrotic changes, contribute to the beneficial effects of curcumin in attenuating the pathogenesis of fatty liver induced metabolic diseases.

scholarly journals Response of Cardiac Tissue Oxidative Stress After Aerobic Exercise and Capsaicin Administrations in Rats Fed High-Fat Diet

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Maryam Davaran ◽  
Ahmad Abdi ◽  
Javad Mehrabani ◽  
Asieh Abbassi Daloii
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Cardiac Tissue ◽  
Aerobic Training ◽  
Normal Diet ◽  
High Fat ◽  
Male Wistar Rats ◽  
Oxidative Effects ◽  
Antioxidant Effects

Background: Oxidative stress harms cells and impairs the balance between oxidative and antioxidative factors. Exercise and capsaicin have anti-inflammatory and antioxidant effects, as well as some benefits on the cardiovascular system. Objectives: The aim of the present study was to examine the effect of aerobic training with capsaicin on heart changes oxidative stress in rats fed a high-fat diet (HFD). Methods: In this experimental study, 40 male Wistar rats were fed a normal diet (ND, n = 8) or HFD (n = 32) for 8 weeks. After eight weeks, all rats were divided into five groups: ND, HFD, high-fat diet-training (HFDT), high-fat diet-capsaicin (HFDCap), high-fat diet-training-capsaicin (HFDTCap). Training groups performed a progressive aerobic running program (at 15 - 25 m/min, 30 - 60 min/day, and 5 days/week) on a motor-driven treadmill for eight weeks. Capsaicin (4 mg/kg/day) was administered orally, by gavage, once a day. Results: The results showed significant increase in cardiac SOD, GPx and CAT levels in HFDT (P < 0.001), HFDCap (P < 0.001) and HFDTCap (P < 0.001) groups. Also, a significant increase in the amount of this index was observed in the HFDTCap compared to the HFDT and HFDCap groups (P < 0.05). The level of malondialdehyde (MDA) in all experimental groups was significantly lower than the HFD group (P < 0.001). Conclusions: Exercise and capsaicin improve HFD-induced oxidative stress. Therefore, exercise and capsaicin can be used as an appropriate alternative treatment for obesity and its associated inflammatory and oxidative effects.

scholarly journals Calorie Restriction with a High-Fat Diet Effectively Attenuated Inflammatory Response and Oxidative Stress-Related Markers in Obese Tissues of the High Diet Fed Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Seungae Park ◽  
Na-Young Park ◽  
Giuseppe Valacchi ◽  
Yunsook Lim
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Calorie Restriction ◽  
High Fat Diet ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Expression Levels ◽  
Diet Induced Obesity ◽  
And Oxidative Stress

Obesity characterized by increased mass of adipose tissue leads to systemic inflammation. Calorie restriction (CR) improves parameters associated with immune response and antioxidant defense. We hypothesized that CR with a high fat diet (HFCR) regulates local and systemic inflammation and oxidative stress damage in a high fat diet induced obesity (HF group). We investigated effect of HFCR on inflammation and oxidative stress-related markers in liver and adipose tissues as well as adipokines in plasma. HFCR lowered liver triglyceride levels, total cholesterol levels, and the plasma leptin/adiponectin ratio to normal levels and improved glucose tolerance. HFCR also improved fatty liver and normalized adipocyte size and morphology. HFCR reduced lipid peroxidation and decreased the expression levels of inducible nitric oxide synthetase, cyclooxygenase-2, NF-E2-related factor, and heme oxygenase-1 in the liver. Moreover, HFCR suppressed the expression levels of C- reactive protein and manganese superoxide dismutase in the adipose tissue in the HF group. These results suggest that HFCR may have beneficial effects on inflammation and oxidative stress as well as lipid profiles in the HF diet induced obesity. Moreover, HFCR may be a good way to increase compliance in obese patients and to prevent obesity induced complications without changes in dietary pattern.

scholarly journals Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Vol 21 (19) ◽  
pp. 7068
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
High Fat Diet ◽  
Intermittent Hypoxia ◽  
Environmental Changes ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are currently no ARHL animal models that can be stimulated by intermittent environmental changes. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined on the basis of expression of hearing-loss-induced phenotypes and aging-related factors. The incidence of hearing loss was significantly higher in dual- and triple-exposure conditions than in intermittent hypoxic conditions, high-fat diet (HFD), or d-galactose injection alone. Continuous oxidative stress and HFD accelerated cellular aging. An increase in Ucp2, usually expressed during mitochondrial dysfunction, was observed. Expression of Cdh23, Slc26a4, Kcnq4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in the cells of the hearing organ. We found that intermittent hypoxia, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects the effects of intermittent environmental changes, will benefit future research on ARHL.

scholarly journals Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly. It is associated with aging and hair cell death due to oxidative stress-induced mitochondrial dysfunction. Although transgenic mice and long-term cultures for induction of aging have been used to study ARHL, there are presently no ARHL animal models stimulated by intermittent environmental change for aging. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined based on the expression of the hearing loss-induced phenotype and aging related factors in the short term. The incidence of hearing loss was significantly different among the groups subjected to intermittent hypoxic environment, high-fat diet (HFD), and injection with D-galactose. Continuous oxidative stress and HFD were factors that accelerated cellular aging. Increase in UCP2 affected oxidative stress and mitochondrial dysfunction. CDH23, SLC26A4, KCNQ4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in cells of the hearing organ. We found that intermittent hypoxic, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects intermittent environmental changes, will benefit future research on ARHL.

Hesperetin ameliorates hepatic oxidative stress and inflammation via the PI3K/AKT-Nrf2-ARE pathway in oleic acid-induced HepG2 cells and a rat model of high-fat diet-induced NAFLD

2021 ◽  
Author(s):  
Jingda Li ◽  
Tianqi Wang ◽  
Panpan Liu ◽  
Fuyuan Yang ◽  
Xudong Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Rat Model ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Citrus Fruits ◽  
High Fat ◽  
Hepatic Oxidative Stress

Hesperetin as a major bioflavonoid in citrus fruits improves NAFLD by suppressing hepatic oxidative stress and inflammation.

Hyperbaric oxygen therapy attenuates D-galactose-induced-age-related cardiac dysfunction through mitigating cardiac mitochondrial dysfunction in pre-diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bo-Htay ◽  
T Shwe ◽  
S Palee ◽  
T Pattarasakulchai ◽  
K Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Lv Function ◽  
High Fat ◽  
Insulin Resistant ◽  
Lv Dysfunction ◽  
Age Related ◽  
Mitochondrial Functions

Abstract Background D-galactose (D-gal) induced ageing has been shown to exacerbate left ventricular (LV) dysfunction via worsening of apoptosis and mitochondrial dysfunction in the heart of obese rats. Hyperbaric oxygen therapy (HBOT) has been demonstrated to exert anti-inflammatory and anti-apoptotic effects in multiple neurological disorders. However, the cardioprotective effect of HBOT on inflammation, apoptosis, LV and mitochondrial functions in D-gal induced ageing rats in the presence of obese-insulin resistant condition has never been investigated. Purpose We sought to determine the effect of HBOT on inflammation, apoptosis, mitochondrial functions and LV function in pre-diabetic rats with D-gal induced ageing. We hypothesized that HBOT attenuates D-gal induced cardiac mitochondrial dysfunctions and reduces inflammation and apoptosis, leading to improved LV function in pre-diabetic rats. Methods Forty-eight male Wistar rats were fed with either normal diet or high-fat diet for 12 weeks. Then, rats were treated with either vehicle groups (0.9% NSS, subcutaneous injection (SC)) or D-gal groups (150 mg/kg/day, SC) for 8 weeks. At week 21, rats in each group were equally divided into 6 sub-groups: normal diet fed rats treated with vehicle (NDV) sham, normal diet fed rats treated with D-gal (NDDg) sham, high fat diet fed rats treated with D-gal (HFDg) sham, high fat diet fed rats treated with vehicle (HFV) + HBOT, NDDg + HBOT and HFDg + HBOT. Sham treated rats were given normal concentration of O2 (flow rate of 80 L/min, 1 ATA for 60 minutes), whereas HBOT treated rats were subjected to 100% O2 (flow rate of 250 L/min, 2 ATA for 60 minutes), given once daily for 2 weeks. Results Under obese-insulin resistant condition, D-gal-induced ageing aggravated LV dysfunction (Fig 1A) and impaired cardiac mitochondrial function, increased cardiac inflammatory and apoptotic markers (Fig 1B). HBOT markedly reduced cardiac TNF-α level and TUNEL positive apoptotic cells, and improved cardiac mitochondrial function as indicated by decreased mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, resulting in the restoration of the normal LV function in HFV and NDDg rats, compared to sham NDDg rats. In addition, in HFDg treated rats, HBOT attenuated cardiac TNF-α level, TUNEL positive apoptotic cells and cardiac mitochondrial dysfunction, compared to sham HFDg rats, leading to improved cardiac function as indicated by increased %LV ejection fraction (LVEF) (Figure 1). Conclusion HBOT efficiently alleviates D-gal-induced-age-related LV dysfunction through mitigating inflammation, apoptosis and mitochondrial dysfunction in pre-diabetic rats. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): 1. The National Science and Technology Development Agency Thailand, 2. Thailand Research Fund Grants

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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