Inhibition of NFκB Activation with Curcumin Attenuates Plasma Inflammatory Cytokines Surge and Cardiomyocytic Apoptosis Following Cardiac Ischemia/Reperfusion1

Yeh, Chi-Hsiao; Chen, Tzu-Ping; Wu, Yi‐Cheng; Lin, Yu‐Min; Lin, Pyng Jing

doi:10.1016/j.jss.2004.11.009

Cited by 111 publications

(78 citation statements)

References 29 publications

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“…Pre-treatment with curcumin was found to markedly attenuate the I/R-induced acute lung injury, probably through improving the oxidative stress (27). Furthermore, it has been shown that curcumin exerts a protective effect in several models of oxidant damage (28-30) including isoproterenolinduced cardiac injury (31) and I/R injury in rabbits (13). Moreover, seven days of oral curcumin supplementation (3.6 g/d) has been shown to decrease the number of oxidative DNA adducts in malignant colorectal tissue suggesting that curcumin taken orally may reach suffi cient concentrations in the gastrointestinal tract (32).…”

Section: Discussionmentioning

confidence: 99%

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Role of curcumin in mesenteric ischemia – reperfusion injury in rats

Okudan²,

Belviranlı³

et al. 2012

BLL

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Abstract:Background: Curcumin is an antioxidant molecule that has been shown to attenuate ischemia/reperfusion (I/R) injury in several organ systems. In the present study, we aimed to evaluate the possible effects of curcumin on contractile response to agonists and histopathological alterations in rat esophagus subjected to mesenteric I/R. Materials and methods: Adult male Wistar albino rats were randomly allocated to 4 groups, namely group I: sham-operated animals (n=10); group II: animals subdued to I/R injury only (n=10) and laparotomy; 45 minutes of superior mesenteric artery ligation were followed by 2 hours of reperfusion, group III: curcumin/sham (n=10); 20 days before I/R, curcumin (200 mg/kg/) was administered by gastric gavage, and group IV: curcumin-I/R (n=10). Mesenteric ischemia/reperfusion model was generated by clamping the superior mesenteric artery for 45 min followed by reperfusion for 2 h. Oral administration of curcumin by gavage at a dose of 200 mg/kg/day lasted 20 days just before inducing the mesenteric ischemia. At the end of reperfusion period, all animals were sacrifi ced and esophagus samples were collected to assess the contractile response to agonists and histopathological alterations. Results: Ischemia/reperfusion signifi cantly decreased the contractile responses to carbachol and KCl and this decrease was attenuated by curcumin. Pretreatment with curcumin caused a remarkable decrease in histopathological parameters such as edema, congestion and infl ammatory cells. Conclusions:The results of the present study demonstrate for the fi rst time that curcumin can attenuate the esophageal injury associated with I/R (Tab. 4, Fig. 3, Ref. 32). Full Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 99%

“…It has been shown to attenuate I/R injury in several organ systems. Recently, it has been reported that curcumin administration ameliorated I/R injury in rat kidney, myocardium, and nervous tissue (13). Curcumin treatment has been recently shown to attenuate reperfusion injury in a superior mesenteric artery I/R model in rats (14).…”

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confidence: 99%

Role of curcumin in mesenteric ischemia – reperfusion injury in rats

Okudan²,

Belviranlı³

et al. 2012

BLL

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“…• Decreased the elevations in plasma IL-8, IL-10 and TNF-a in rabbits after cardiopulmonary bypass and cardiac global ischaemia (Yeh et al, 2005).…”

Section: Figurementioning

confidence: 99%

“…down-regulate NF-kB-regulated gene products such as inducible NOS (iNOS), IL-1, IL-6, IL-8, MCP-1, MMP-2 and MMP-9 in animals (Yao et al, 2004;Yeh et al, 2005;Jain et al, 2009). Curcumin also protects against the toxic effects of copper overload (Wan et al, 2007), dextran sulfate sodium (Arafa et al, 2009), p-dioxin (Ciftci et al, 2010) and aluminum (Sood et al, 2011) through down-modulation of TNF-a.…”

Section: Figurementioning

confidence: 99%

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

Aggarwal

Gupta

Sung

2013

British J Pharmacology

337

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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“…The effect was closely related to the inhibition of I/R-induced inflammatory reaction. Previous studies (Yeh et al, 2005;Liu et al, 2006b) have shown that I/R induced the overexpression of TNF-a, IL-1, IL-6, and other proinflammatory cytokines through activation of nuclear factor (NF)-kappaB protein expression to cause the inflammatory response of myocardial injury. The downregulation of NF-kappaB protein expression could inhibit the over expression of TNF-a, IL-1, IL-6, and other proinflammatory cytokines and raise the expression of IL-10 to eventually reduce the infarction size.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of morphine preconditioning in delayed phase on myocardial ischemia-reperfusion injury in rabbits

Lu¹,

K²,

Yy³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to investigate the protective mechanisms of delayed-phase morphine preconditioning on myocardial ischemia-reperfusion injury. Thirty healthy male New Zealand white rabbits were randomly divided into three groups: a sham operation group (C), ischemia-reperfusion group (I/R), and delayed-phase morphine preconditioning group (M) (N = 10/group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group received left artery blockage for 40 min and reperfusion for 120 min. Rabbits in the M group received 1.0 mg/kg intravenous morphine 24 h prior to the identical treatment as the rabbits in the I/R group. In each group, the interleukin (IL)-10 and tumor necrosis factor (TNF)-α levels were detected at five time points: 20 min before the left coronary artery blockage (T1), 20 and 40 min after the left coronary artery blockage (T2 and T3, respectively), and 1 and 2 h after the myocardial reperfusion (T4 and T5, respectively). After reperfusion, the infarction size was 8948 X.-H. Lu et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 8947-8954 (2015) measured with Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Compared with the C group, serum IL-10 and TNF-α concentrations increased in the I/R and M groups; the difference was significant (P < 0.05). When compared with the I/R group, the IL-10 concentrations in the M group were significantly increased (P < 0.05), but the infarction size and TNF-α concentrations were significantly decreased (P < 0.05). These results suggested that delayed-phase morphine preconditioning might achieve myocardial protection through the regulation and balance of inflammatory cytokines.

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Inhibition of NFκB Activation with Curcumin Attenuates Plasma Inflammatory Cytokines Surge and Cardiomyocytic Apoptosis Following Cardiac Ischemia/Reperfusion1

Cited by 111 publications

References 29 publications

Role of curcumin in mesenteric ischemia – reperfusion injury in rats

Role of curcumin in mesenteric ischemia – reperfusion injury in rats

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

Protective effects of morphine preconditioning in delayed phase on myocardial ischemia-reperfusion injury in rabbits

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