The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury

Önder, Akın; Kapan, Murat; Gümüş, Metehan; Yüksel, Hatice; Böyük, Abdullah; Alp, Harun; Başarili, Mustafa Kemal; Fırat, Uğur

doi:10.4318/tjg.2012.0446

Cited by 32 publications

(25 citation statements)

References 25 publications

(24 reference statements)

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“…Having the established advantage of safe and slight adverse effects, curcumin provides a novel therapeutic approach that merits further exploration. There is a wealth of experimental evidence suggesting that multiple mechanisms of action are likely responsible for the various pharmacological effects of curcumin on stress-related signaling molecules [6–8]. These include modulation of NF- κ B and its target molecule, such TNF- α and ICAM-1, and other oxidative and antioxidative enzymes involved in I/R stress.…”

Section: Discussionmentioning

confidence: 99%

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The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

Jing

Yao

et al. 2014

Oxidative Medicine and Cellular Longevity

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Objective. In this study, we investigated the protective effect and mechanism of curcumin on a rat model of intestinal ischemia/reperfusion (I/R), which induces an acute liver lesion. Methods. Curcumin was injected into rats in the curcumin groups through left femoral vein. The same volume of vehicle (0.9% normal saline) was injected into sham and I/R groups. Blood and liver tissue were gathered for serological and histopathological determination. Results. Intestinal I/R led to severe liver injury manifested as a significant increase in serum AST and ALT levels; all of those were reduced by treatment with curcumin. Simultaneously, the activity of SOD in liver decreased after intestinal I/R, which was increased by curcumin treatment. On the other hand, curcumin reduced MPO activity of liver tissue, as well as serum IL-6 and TNF-α levels observably. This is in parallel with the decreased level of liver intercellular cell adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NF-κB) expression. Conclusion. Our findings suggest that curcumin treatment attenuates liver lesion induced by intestinal I/R, attributable to the antioxidative and anti-inflammatory effect via inhibition of the NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

“…Curcumin is antineoplastic and anti-inflammatory including anti-I/R [5–7]. However, the potential protective mechanism of curcumin on acute liver lesion induced by intestinal I/R still needs to be further explored [8]. …”

Section: Introductionmentioning

confidence: 99%

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

Jing

Yao

et al. 2014

Oxidative Medicine and Cellular Longevity

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“…Curcumin is associated with regulation of several antioxidant genes by restoring their activity and expression levels (1,12,15,61). Curcumin is known to enhance the cellular antioxidant defense system using different pathways including NF-B and thereby protect cells against oxidative stress (71). We think that curcumin may enhance the Prdx6 expression in neuronal cells by optimizing activity of NF-B, a regulator of Prdx6 gene during stress.…”

mentioning

confidence: 99%

“…However, the proapoptotic and antiapoptotic roles of NF-B depend on cell types and cellular microenvironment as well as levels of intracellular ROS (69). Moreover, curcumin, a biologically active component of turmeric (Curcuma longa), has a variety of anticarcinogenic, antibacterial, antifungal, antiviral, anti-inflammatory, antiproliferative, and antiapoptotic effects (56,65,71,73). Curcumin is associated with regulation of several antioxidant genes by restoring their activity and expression levels (1,12,15,61).…”

mentioning

confidence: 99%

Curcumin abates hypoxia-induced oxidative stress based-ER stress-mediated cell death in mouse hippocampal cells (HT22) by controlling Prdx6 and NF-κB regulation

Chhunchha

Fatma

Kubo

et al. 2013

American Journal of Physiology-Cell Physiology

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Oxidative stress and endoplasmic reticulum (ER) stress are emerging as crucial events in the etiopathology of many neurodegenerative diseases. While the neuroprotective contributions of the dietary compound curcumin has been recognized, the molecular mechanisms underlying curcumin's neuroprotection under oxidative and ER stresses remains elusive. Herein, we show that curcumin protects HT22 from oxidative and ER stresses evoked by the hypoxia (1% O(2) or CoCl(2) treatment) by enhancing peroxiredoxin 6 (Prdx6) expression. Cells exposed to CoCl(2) displayed reduced expression of Prdx6 with higher reactive oxygen species (ROS) expression and activation of NF-κB with IκB phosphorylation. When NF-κB activity was blocked by using SN50, an inhibitor of NF-κB, or cells treated with curcumin, the repression of Prdx6 expression was restored, suggesting the involvement of NF-κB in modulating Prdx6 expression. These cells were enriched with an accumulation of ER stress proteins, C/EBP homologous protein (CHOP), GRP/78, and calreticulin, and had activated states of caspases 12, 9, and 3. Reinforced expression of Prdx6 in HT22 cells by curcumin reestablished survival signaling by reducing propagation of ROS and blunting ER stress signaling. Intriguingly, knockdown of Prdx6 by antisense revealed that loss of Prdx6 contributed to cell death by sustaining enhanced levels of ER stress-responsive proapoptotic proteins, which was due to elevated ROS production, suggesting that Prdx6 deficiency is a cause of initiation of ROS-mediated ER stress-induced apoptosis. We propose that using curcumin to reinforce the naturally occurring Prdx6 expression and attenuate ROS-based ER stress and NF-κB-mediated aberrant signaling improves cell survival and may provide an avenue to treat and/or postpone diseases associated with ROS or ER stress.

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“…Other studies showed increased MDA levels after 60 min of reperfusion in rats following 60 or 45 min of SMA occlusion (23,24). Önder et al reported a significant increase in serum MDA levels in a mesenteric I/R injury model of 30 min of ischemia followed by a 1-h reperfusion period (25). The authors concluded that curcumin ameliorated histopathological damage in the intestine and distant organs and prevented the increase in serum MDA levels with mesenteric I/R injury.…”

Section: Discussionmentioning

confidence: 94%

Protective effects of montelukast and Hypericum perforatum against intestinal ischemia-reperfusion injury in hamsters

Ocak¹,

Duran²,

Özyalvaçli³

et al. 2014

Turk J Med Sci

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The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury

Cited by 32 publications

References 25 publications

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

The Protective Effects of Curcumin on Experimental Acute Liver Lesion Induced by Intestinal Ischemia-Reperfusion through Inhibiting the Pathway of NF-κB in a Rat Model

Curcumin abates hypoxia-induced oxidative stress based-ER stress-mediated cell death in mouse hippocampal cells (HT22) by controlling Prdx6 and NF-κB regulation

Protective effects of montelukast and Hypericum perforatum against intestinal ischemia-reperfusion injury in hamsters

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