Curcumin, a polyphenolic antioxidant, attenuates chronic fatigue syndrome in murine water immersion stress model

Gupta, Amit K.; Vij, Garima; Sharma, Sameer; Tirkey, Naveen; Rishi, Praveen; Chopra, Kanwaljit

doi:10.1016/j.imbio.2008.04.003

Cited by 69 publications

(57 citation statements)

References 37 publications

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“…Decreased TNF-a levels have also been noted in tumour-bearing animals treated with this polyphenol (Leyon and Kuttan, 2003). In addition to cancer, down-regulation of TNF-a by curcumin has been associated with protection from various pro-inflammatory diseases, including sub-chronic inflammation (Nandal et al, 2009;Nishida et al, 2010), cardiovascular diseases (Yao et al, 2004;Mito et al, 2011;Avci et al, 2012), diabetes (Jain et al, 2009;El-Azab et al, 2011;El-Moselhy et al, 2011), acute pancreatitis (Gulcubuk et al, 2006), enterocolitis (Jia et al, 2010), enteritis (Song et al, 2010), prostatitis (Zhang et al, 2010b), diabetic neuropathy (Sharma et al, 2007b), hepatic injury (Yun et al, 2010), Th1-type ileitis (Bereswill et al, 2010), hepatic fibrosis (Shu et al, 2007;Zeng et al, 2011), radiationinduced lung fibrosis , asthma (Ammar el et al, 2011), alcohol-induced liver disease (Nanji et al, 2003), non-alcoholic steatohepatitis (Ramirez-Tortosa et al, 2009), concanavalin A-induced liver injury (Tu et al, 2012), renal injury (Hashem et al, 2008;Pan et al, 2012), infection (Allam, 2009), fatigue (Gupta et al, 2009), bone turnover (Yang et al, 2011) and high-fat diet-induced hyperglycaemia (El-Moselhy et al, 2011). Curcumin has also been found to…”

Section: Suppression Of Tnf By Curcumin In Vivomentioning

confidence: 99%

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Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

343

239

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TNFs are major mediators of inflammation and inflammation-related diseases, hence, the United States Food and Drug Administration (FDA) has approved the use of blockers of the cytokine, TNF-a, for the treatment of osteoarthritis, inflammatory bowel disease, psoriasis and ankylosis. These drugs include the chimeric TNF antibody (infliximab), humanized TNF-a antibody (Humira) and soluble TNF receptor-II (Enbrel) and are associated with a total cumulative market value of more than $20 billion a year. As well as being expensive ($15 000-20 000 per person per year), these drugs have to be injected and have enough adverse effects to be given a black label warning by the FDA. In the current report, we describe an alternative, curcumin (diferuloylmethane), a component of turmeric (Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-a action and production in in vitro models, in animal models and in humans. In addition, we provide evidence for curcumin's activities against all of the diseases for which TNF blockers are currently being used. Mechanisms by which curcumin inhibits the production and the cell signalling pathways activated by this cytokine are also discussed. With health-care costs and safety being major issues today, this golden spice may help provide the solution. LINKED ARTICLESThis article is part of a themed section on Emerging Therapeutic Aspects in Oncology. To view the other articles in this section visit http://dx

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Section: Suppression Of Tnf By Curcumin In Vivomentioning

confidence: 99%

“…• Significantly attenuated oxidative stress and TNF-a levels in a mouse model of immunologically induced fatigue (Gupta et al, 2009). …”

Section: Figurementioning

confidence: 99%

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Aggarwal

Gupta

Sung

2013

British J Pharmacology

343

239

View full text Add to dashboard Cite

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“…The oxidative stress thus generated, induces a rapid alteration in the antioxidant systems by depleting the cellular stores of endogenous antioxidants such as superoxide dismutase, catalase, glutathione and vitamin E [1,11,12]. One approach to combat the bacterial product-induced oxidative stress is the use of antioxidant treatments through intraperitoneal, intravenous, or dietary administration [2,13].…”

Section: Introductionmentioning

confidence: 99%

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Bharrhan¹,

Chopra²,

Rishi³

2010

Am. J. Biomed. Sci.

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Vitamin E (-Tocopherol [-Toc]) is the primary membrane bound, lipid-soluble, chain-breaking antioxidant that has been reported to protect against lipid peroxidation-induced tissue damage. Therefore, the present study was designed to investigate the protection afforded by α-Tocopherol (vitamin E), if any, on LPS-induced liver injury in Wistar rats and to study the underlying mechanism of protection. Bacterial endotoxin (10 mg/Kg body weight-prestandardized dose) was injected intraperitoneally and animals were sacrificed 8 h post-challenge. Vitamin E (35 mg/Kg body weight) was administered orally for 15 days prior to endotoxin challenge. Challenge with LPS resulted in a significant increase in the activities of serum transaminases and alkaline phosphatase along with histological alterations in the liver. These responses were associated with elevated levels of malondialdehyde (MDA) and reduced levels of glutathione, superoxide dismutase and catalase along with increased levels of tumor necrosis factor alpha (TNF-α) in the liver homogenates. However, vitamin E supplementation attenuated the oxidative stress by reducing the levels of MDA, restoring the levels of glutathione, superoxide dismutase and catalase and decreasing the levels of TNF-α. Decreased TNF-α levels after vitamin E supplementation might have resulted into the modulation of above mentioned biochemical changes resulting into amelioration of hepatic architecture. Vitamin E, therefore, seems to have a promising role for clinical manifestations due to oxidative stress.

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“…There is no immediate treatment available for the effective management of this disease. However, plenty of evidence suggest the potential beneficial effects of antioxidants in the management of chronic fatigue and related problems (Singh et al 2002;Singal et al 2005;Gupta et al 2009). …”

Section: Introductionmentioning

confidence: 99%

Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice

2010

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Chronic fatigue is an illness characterised by persistent and relapsing fatigue, often accompanied by numerous neuropsychiatric problems, such as anxiety and depression. The aetiology of chronic fatigue remains unclear so far. However, recent studies suggested the involvement of oxidative stress in this chronic debilitating disease. Alternatively, antioxidants have also been reported to have beneficial effect against chronic fatigue-like conditions. Therefore, present study has been designed to explore the potential role of pioglitazone, caffeic acid and their combination against chronic fatigue-like condition in mice. In the experimental protocol, the mice were put on the running wheel apparatus for 6 min test session daily for 21 days which produced fatigue-like condition. The locomotor activity and anxiety levels were measured on 0, 8th, 15th and 22nd days. The brains were isolated on 22nd day immediately after the behavioural assessments, oxidative damage and mitochondrial enzyme complexes were then estimated subsequently. Three weeks pioglitazone (5 and 10 mg/kg) and caffeic acid (5 and 10 mg/kg) pretreatment significantly attenuated the chronic fatigue-like condition (restored running wheel activity, locomotor activity and reduced anxiety-like behaviour) as compared to that in control (chronic fatigue) animals. Further, pioglitazone (5 and 10 mg/kg) and caffeic acid (5 and 10 mg/kg) drug treatments for 3 weeks significantly attenuated oxidative damage (decreased lipid peroxidation, nitrite concentration, restored reduction in glutathione and catalase levels), altered mitochondrial enzymes complex (I, II and IV) activities and mitochondrial redox activity (MTT assay) when compared with control. Further, combination of lower dose of pioglitazone (5 mg/kg) and caffeic acid (5 mg/kg) showed significant synergism in their protective effect which was significant as compared to their effect per se. The present study highlights the potential role of pioglitazone, caffeic acid and their combination in the pathophysiology of chronic fatigue-like condition in mice.

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Curcumin, a polyphenolic antioxidant, attenuates chronic fatigue syndrome in murine water immersion stress model

Cited by 69 publications

References 37 publications

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Curcumin: an orally bioavailable blocker of TNF and other pro‐inflammatory biomarkers

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice

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