Curcumin Attenuates Renal Ischemia and Reperfusion Injury–Induced Restrictive Respiratory Insufficiency

Yeh, Jih-Chen; Yang, Y.-C.; Wang, J.-C.; Wang, D.

doi:10.1016/j.transproceed.2013.09.004

Cited by 14 publications

(11 citation statements)

References 12 publications

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“…Ischemia causes oxidative stress reflected by the generation of MDA in the affected tissues (36,37). Similar to previous reports (38,39), our study confirmed increased generation of MDA in ischemia and this was inhibited by the cathepsin inhibitor E64d.…”

Section: Discussionsupporting

confidence: 92%

Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia

Satyam

Kannan

Matsumoto

et al. 2017

The Journal of Immunology

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Intestinal ischemia followed by reperfusion leads to local and remote organ injury attributed to inflammatory response during the reperfusion phase. The extent to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly studied. After careful evaluation of intestinal tissue following 30 min of ischemia, we noticed significant local mucosal injury in wild-type mice. This injury was drastically reduced in C3-deficient mice, suggesting C3 involvement. Depletion of circulating complement with cobra venom factor eliminated, as expected, injury recorded at the end of the reperfusion phase but failed to eliminate injury that occurred during the ischemic phase. Immunohistochemical studies showed that tissue damage during ischemia was associated with increased expression of C3/C3 fragments primarily in the intestinal epithelial cells, suggesting local involvement of complement. In vitro studies using Caco2 intestinal epithelial cells showed that in the presence of LPS or exposure to hypoxic conditions the cells produce higher C3 mRNA as well as C3a fragment. Caco2 cells were also noted to produce cathepsins B and L, and inhibition of cathepsins suppressed the release of C3a. Finally, we found that mice treated with a cathepsin inhibitor and cathepsin B-deficient mice suffer limited intestinal injury during the ischemic phase. To our knowledge, our findings demonstrate for the first time that significant intestinal injury occurs during ischemia prior to reperfusion and that this is due to activation of C3 within the intestinal epithelial cells in a cathepsin-dependent manner. Modulation of cathepsin activity may prevent injury of organs exposed to ischemia.

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Section: Discussionsupporting

confidence: 92%

Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia

Satyam

Kannan

Matsumoto

et al. 2017

The Journal of Immunology

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“…Curcumin is an antioxidant molecule (49) that protects against renal damage associated with AKI, as reported in gentamicin-or cisplatin-induced nephrotoxicity and ischemia-reperfusion injury (22,50,51). However, the protective effects of curcumin in rhabdomyolysis-AKI are not clear.…”

Section: Discussionmentioning

confidence: 99%

Curcumin reduces renal damage associated with rhabdomyolysis by decreasing ferroptosis‐mediated cell death

et al. 2019

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Acute kidney injury is a common complication of rhabdomyolysis. A better understanding of this syndrome may be useful to identify novel therapeutic targets because there is no specific treatment so far. Ferroptosis is an iron‐dependent form of regulated nonapoptotic cell death that is involved in renal injury. In this study, we investigated whether ferroptosis is associated with rhabdomyolysis‐mediated renal damage, and we studied the therapeutic effect of curcumin, a powerful antioxidant with renoprotective properties. Induction of rhabdomyolysis in mice increased serum creatinine levels, endothelial damage, inflammatory chemokines, and cytokine expression, alteration of redox balance (increased lipid peroxidation and decreased antioxidant defenses), and tubular cell death. Treatment with curcumin initiated before or after rhabdomyolysis induction ameliorated all these pathologic and molecular alterations. Although apoptosis or receptor‐interacting protein kinase (RIPK)3‐mediated necroptosis were activated in rhabdomyolysis, our results suggest a key role of ferroptosis. Thus, treatment with ferrostatin 1, a ferroptosis inhibitor, improved renal function in glycerol‐injected mice, whereas no beneficial effects were observed with the pan‐caspase inhibitor carbobenzoxy‐valyl‐alanyl‐aspartyl‐(O‐methyl)‐fluoromethylketone or in RIPK3‐deficient mice. In cultured renal tubular cells, myoglobin (Mb) induced ferroptosis‐sensitive cell death that was also inhibited by curcumin. Mechanistic in vitro studies showed that curcumin reduced Mb‐mediated inflammation and oxidative stress by inhibiting the TLR4/NF‐κB axis and activating the cytoprotective enzyme heme oxygenase 1. Our findings are the first to demonstrate the involvement of ferroptosis in rhabdomyolysis‐associated renal damage and its sensitivity to curcumin treatment. Therefore, curcumin may be a potential therapeutic approach for patients with this syndrome.—Guerrero‐Hue, M., García‐Caballero, C., Palomino‐Antolín, A., Rubio‐Navarro, A., Vázquez‐Carballo, C., Herencia, C., Martín‐Sanchez, D., Farré‐Alins, V., Egea, J., Cannata, P., Praga, M., Ortiz, A., Egido, J., Sanz, A. B., Moreno, J. A. Curcumin reduces renal damage associated with rhabdomyolysis by decreasing ferroptosis‐mediated cell death. FASEB J. 33,8961–8975 (2019). http://www.fasebj.org

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“…Curcumin is a yellow colored polyphenolic compound derived from Curcuma longa. More and more research proves that curcumin could exert a variety of pharmacological and biological properties [ 12 – 13 ]. There have been three articles reporting of the effects of curcumin on kidney and myocardial I/R injury, however, the impact of curcumin on hepatic I/R has not been investigated.…”

Section: Discussionmentioning

confidence: 99%

Curcumin protects against hepatic ischemia/reperfusion induced injury through inhibiting TLR4/NF-κB pathway

Wang

Lin

et al. 2017

Oncotarget

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The TLR4/NF-κB pathway had important roles in hepatic ischemia/reperfusion (I/R) injury. In this study, we reported a protective effect of curcumin against hepatic I/R injury via TLR4/NF-κB pathway. Curcumin significantly inhibited cell apoptosis, and decreased levels of LDH and production of TNF-a, IL-1b, and IL-6 in the cell supernatant. In addition, curcumin ameliorated elevated TLR4 and NF-κB caused by hypoxia/reoxygenation stimulation in BRL-3A cells. In vivo assays revealed that curcumin reduce levels of ALT and AST, and reversed TLR4/NF-κB signaling pathway caused by hepatic I/R stimulation in liver tissues. These results suggested that curcumin ameliorates hepatic I/R injury, which may be mediated in part via the TLR4/NF-κB signaling pathway.

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Curcumin Attenuates Renal Ischemia and Reperfusion Injury–Induced Restrictive Respiratory Insufficiency

Cited by 14 publications

References 12 publications

Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia

Intracellular Activation of Complement 3 Is Responsible for Intestinal Tissue Damage during Mesenteric Ischemia

Curcumin reduces renal damage associated with rhabdomyolysis by decreasing ferroptosis‐mediated cell death

Curcumin protects against hepatic ischemia/reperfusion induced injury through inhibiting TLR4/NF-κB pathway

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