Curcumin reduces the cardiac ischemia–reperfusion injury: involvement of the toll-like receptor 2 in cardiomyocytes

Kim, Yong Sook; Kwon, Jin-Sook; Cho, Young Kuk; Jeong, Myung Ho; Cho, Jeong Gwan; Park, Jong Chun; Kang, Jung Chaee

doi:10.1016/j.jnutbio.2011.10.004

Cited by 57 publications

(58 citation statements)

References 36 publications

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“…In addition, curcumin has been demonstrated to have a suppressive effect against the apoptosis by suppression of caspase-3 and TGF-β [25]. In fact, a lot of studies have demonstrated that curcumin prevents against inflammation, oxidative stress, tissue damages and functional disturbances resulted from RIRI in the kidney and other organs [9, 26]. The application of curcumin in this study resulted in partially restored kidney function and less damages to renal tubules, as well an overall inactivation of iNOS/NO/cGMP/PKG signaling pathway [27].…”

Section: Discussionmentioning

confidence: 99%

Administration of Curcumin Protects Kidney Tubules Against Renal Ischemia-Reperfusion Injury (RIRI) by Modulating Nitric Oxide (NO) Signaling Pathway

Liu

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: To explore the protective effect of curcumin on renal ischemia-reperfusion injury (RIRI) in rats, and its influence on nephridial tissue’s NO and cGMP levels as well as downstream signaling pathway, to elucidate the possible mechanism of curcumin on RIRI. Methods: 36 Sprague Dawley rats (SD rats) were randomly divided into Sham group, Model group, curcumin (CUR +) Model group, 12 rats per group. They were all given RIRI model preparation by unilateral artery occlusion method. All groups’ β2-MG in urine in 24h, serum Cr and BUN were compared, and UAER were calculated. Nitric oxide synthase (NOS), cGMP-dependent protein kinase (PKG), Caspase-3 expression were all determined by western blot. Nitric oxide (NO), NOS and cGMP levels were also examined by using ELISA. All groups’ nephridial histomorphology and kidney tubules score were evaluated and compared. Results: β2-MG and UAER in urine, serum Cr and BUN, in renal tissue were all elevated in Model of RIRI, indicating the success of animal model of RIRI establishment, and above index in CUR + Model group were all lower than those in Model group. Furthermore, iNOS, NO, cGMP, PKG and Caspase-3 in renal tissue were all increased in Model of RIRI, indicating the NO signaling pathway was activated, which is one of the pathogenesis of RIRI, and above index in CUR + Model group were all lower than those in Model group, suggesting that inactivation of iNOS/NO/cGMP/PKG signaling pathway is one of the reasons that explain the protective effect of curcumin in RIRI. Conclusion: The activation of iNOS/NO/cGMP/PKG signaling pathway and the consequent promoted apoptosis of renal tubules are significantly involved in the pathogenesis of development of RIRI, and curcumin treatment could protect renal tubules against RIRI, at least partially, by suppressing the activated iNOS/NO/cGMP/PKG signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Administration of Curcumin Protects Kidney Tubules Against Renal Ischemia-Reperfusion Injury (RIRI) by Modulating Nitric Oxide (NO) Signaling Pathway

Liu

Zhang

et al. 2017

Cell Physiol Biochem

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“…Several of our previous studies have focused on the development of new anti-inflammatory derivatives or analogs of curcumin, the main active component of Curcuma and ginger, which have shown multiple pharmacological activities (19,33). C66, a synthetic curcumin analog developed in our laboratory, has been shown to exert antiinflammatory effects both in vitro and in vivo (20).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of JNK Phosphorylation by a Novel Curcumin Analog Prevents High Glucose–Induced Inflammation and Apoptosis in Cardiomyocytes and the Development of Diabetic Cardiomyopathy

Pan¹,

et al. 2014

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Hyperglycemia-induced inflammation and apoptosis have important roles in the pathogenesis of diabetic cardiomyopathy. We recently found that a novel curcumin derivative, C66, is able to reduce the high glucose (HG)-induced inflammatory response. This study was designed to investigate the protective effects on diabetic cardiomyopathy and its underlying mechanisms. Pretreatment with C66 significantly reduced HG-induced overexpression of inflammatory cytokines via inactivation of nuclear factor-κB in both H9c2 cells and neonatal cardiomyocytes. Furthermore, we showed that the inhibition of Jun NH2-terminal kinase (JNK) phosphorylation contributed to the protection of C66 from inflammation and cell apoptosis, which was validated by the use of SP600125 and dominant-negative JNK. The molecular docking and kinase activity assay confirmed direct binding of C66 to and inhibition of JNK. In mice with type 1 diabetes, the administration of C66 or SP600125 at 5 mg/kg significantly decreased the levels of plasma and cardiac tumor necrosis factor-α, accompanied by decreasing cardiac apoptosis, and, finally, improved histological abnormalities, fibrosis, and cardiac dysfunction without affecting hyperglycemia. Thus, this work demonstrated the therapeutic potential of the JNK-targeting compound C66 for the treatment of diabetic cardiomyopathy. Importantly, we indicated a critical role of JNK in diabetic heart injury, and suggested that JNK inhibition may be a feasible strategy for treating diabetic cardiomyopathy.

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“…Data were analyzed by one-way analysis of variance (one-way ANOVA), and the intergroup differences were detected by Tukey multiple comparison, when p < 0.05. resveratrol protected against CCl 4 hepatotoxicity in rats via the suppression of fibrogenic cytokine release [15]. Similarly, curcumin treatment was found to ameliorate myocardial I/R injury in rats through the inhibition of a toll-like receptor-2-mediated inflammatory response [16].…”

Section: Discussionmentioning

confidence: 98%

Schisandrin B Enhances Hepatic/Myocardial Glutathione Regeneration Capacity and Protects Against Oxidant Injury in Rat Livers and Hearts

Leong¹,

Chen²,

Ko³

2013

TONUTRAJ

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Abstract:The effects of schisandrin B (Sch B), curcumin, epigallocatechin gallate (EGCG) and resveratrol on the glutathione regeneration capacity (GRC) of liver and heart tissues ex vivo were examined in relation to their protective effects against CCl 4 hepatotoxicity in vivo and myocardial ischemia/reperfusion (I/R) injury ex vivo in rats. Results indicated that Sch B, but not curcumin, EGCG or resveratrol, caused hepatic and myocardial GRC enhancement, which was paralleled by its protection against CCl 4 hepatotoxicity and myocardial I/R injury. Although resveratrol and curcumin failed to increase the GRC of liver/heart tissues, they did protect against CCl 4 hepatotoxicity and myocardial I/R injury. In conclusion, the Sch B-induced enhancement of GRC ex vivo correlated well with its ability to protect tissues against oxidant injury in vivo/ex vivo, suggesting that the GRC assay can be used as a monitor of tissue protection for compounds stimulating glutathione redox cycling. However, phytochemicals can also protect against oxidant injury through various other mechanisms.

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Curcumin reduces the cardiac ischemia–reperfusion injury: involvement of the toll-like receptor 2 in cardiomyocytes

Cited by 57 publications

References 36 publications

Administration of Curcumin Protects Kidney Tubules Against Renal Ischemia-Reperfusion Injury (RIRI) by Modulating Nitric Oxide (NO) Signaling Pathway

Administration of Curcumin Protects Kidney Tubules Against Renal Ischemia-Reperfusion Injury (RIRI) by Modulating Nitric Oxide (NO) Signaling Pathway

Inhibition of JNK Phosphorylation by a Novel Curcumin Analog Prevents High Glucose–Induced Inflammation and Apoptosis in Cardiomyocytes and the Development of Diabetic Cardiomyopathy

Schisandrin B Enhances Hepatic/Myocardial Glutathione Regeneration Capacity and Protects Against Oxidant Injury in Rat Livers and Hearts

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