Curcumin prevents cisplatin-induced renal alterations in mitochondrial bioenergetics and dynamic

Ortega-Domínguez, Bibiana; Aparicio-Trejo, Omar Emiliano; García-Arroyo, Fernando E.; León-Contreras, Juan Carlos; Tapia, Edilia; Molina‐Jijón, Eduardo; Hernández-Pando, Rogelio; Sánchez‐Lozada, Laura G.; Barrera-Oviedo, Diana; Pedraza‐Chaverrí, José

doi:10.1016/j.fct.2017.07.018

Cited by 106 publications

(85 citation statements)

References 47 publications

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“…However, curcuminoids exhibit certain disadvantages, including low bioavailability and www.nature.com/scientificreports www.nature.com/scientificreports/ suboptimal pharmacokinetic properties 15,40 . Nanoscale has been proven to be an appropriate strategy to overcome bioavailability limitations and improve the bioactivity of diet-derived phytochemicals and curcumin 16,17,41,42 . Specifically, the use of polymer therapeutics, and the development of polymer-drug conjugates, in particular, provide longer drug half-lives, improve pharmacokinetic/pharmacodynamic properties, and increase drug accumulation within inflamed/diseased/damaged tissues thanks to the enhanced retention and permeability effect 18,43 .…”

Section: Discussionmentioning

confidence: 99%

“…Nanotechnology-based drug carriers, including polymeric micelles, liposomes, polymeric nanoparticles, nanoemulsions, nanosuspensions, and polymer conjugates can enhance the availability and effective therapeutic outcomes of curcuminoids 16,17 . Specifically, polymer therapeutics are "new chemical entities" (nanomedicines with demonstrated clinical benefits) that can overcome the low bioavailability of free drugs through an increased capacity to i) cross biological barriers, ii) reach specific intracellular compartments and iii) optimize pharmacokinetics 18,19 .…”

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confidence: 99%

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Effective Nephroprotection Against Acute Kidney Injury with a Star-Shaped Polyglutamate-Curcuminoid Conjugate

Córdoba-David

Duro‐Castaño

Castelo‐Branco

et al. 2020

Sci Rep

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The lack of effective pharmacological treatments for acute kidney injury (AKI) remains a significant public health problem. Given the involvement of apoptosis and regulated necrosis in the initiation and progression of AKI, the inhibition of cell death may contribute to AKI prevention/recovery. Curcuminoids are a family of plant polyphenols that exhibit attractive biological properties that make them potentially suitable for AKI treatment. Now, in cultured tubular cells, we demonstrated that a crosslinked self-assembled star-shaped polyglutamate (PGA) conjugate of bisdemethoxycurcumin (St-PGA-CL-BDMC) inhibits apoptosis and necroptosis induced by Tweak/TNFα/IFNγ alone or concomitant to caspase inhibition. St-PGA-CL-BDMC also reduced NF-κB activation and subsequent gene transcription. In vivo, St-PGA-CL-BDMC prevented renal cell loss and preserved renal function in mice with folic acid-induced AKI. Mechanistically, St-PGA-CL-BDMC inhibited AKI-induced apoptosis and expression of ferroptosis markers and also decreased the kidney expression of genes involved in tubular damage and inflammation, while preserving the kidney expression of the protective factor, Klotho. Thus, due to renal accumulation and attractive pharmacological properties, the application of PGAbased therapeutics may improve nephroprotective properties of current AKI treatments. Acute kidney injury (AKI) involves a sudden and generally transient loss of glomerular filtration leading to the retention of damaging nitrogenous byproducts normally excreted in the urine. Independently of its etiology, AKI usually implies extensive renal parenchymal injury, which, in the case of unsuccessful repair, favors the progression of AKI to chronic kidney disease (CKD). The mortality of AKI may be as high as 50%, and currently, there exist no specific therapies to attenuate AKI or accelerate recovery beyond dialysis 1. Thus, there is an unmet clinical need for novel AKI treatments. During the initial stages of AKI, proximal renal tubular cell death triggers a cascade of damaging events, including inflammation, that amplifies kidney injury 2,3. Thus, the control and execution of apoptosis and several kinds of regulated necrosis depend on environmental conditions as well as on the recruitment of intracellular cell death pathways. Distinct forms of cell death are amenable to pharmacological modulation. Strategies to specifically inhibit caspases, the final executioners of apoptosis, decrease apoptosis, inflammation, and improve renal function in experimental ischemia/reperfusion or septic AKI 4,5. However, the inhibition of overall caspase activity failed to improve nephrotoxic AKI 6. In this regard, caspase activation is involved in cellular events beyond cell death regulation, including, among others, cell cycle and the regulation of proliferation 7,8. Strategies that interfere with initial or intermediate regulators of caspase activity, like protein kinases, survival factors, cytokine death receptors, oxidative stress factors, apoptosome factors, and tumor-suppresso...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effective Nephroprotection Against Acute Kidney Injury with a Star-Shaped Polyglutamate-Curcuminoid Conjugate

Córdoba-David

Duro‐Castaño

Castelo‐Branco

et al. 2020

Sci Rep

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“…Different mechanisms have been identified in cisplatin-induced renal injury, such as oxidative stress, apoptosis, and mitochondrial damage of renal cells. Therefore, mitochondrial homeostasis is crucial for maintaining renal function and for counteracting kidney injury [72].…”

Section: Kidney Diseasementioning

confidence: 99%

“…In addition, curcumin decreased the expression levels of some mitophagy-associated proteins, such as PINK1 [72].…”

Section: Kidney Diseasementioning

confidence: 99%

Effects of Plant and Animal Natural Products on Mitophagy

Shakeri

Bianconi

Pirro

et al. 2020

Oxidative Medicine and Cellular Longevity

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Mitophagy is a protected cellular process that is essential for autophagic removal of damaged mitochondria and for preservation of a healthy mitochondrial population. In the last years, a particular interest has been devoted in studying the effects of natural compounds on mitophagy. Different natural compounds may modulate mitochondrial oxidative phosphorylation, the production of mitochondrial reactive oxygen species, the expression of mitophagy-and autophagy-related genes, and the activities of transcription factors which regulate the expression of mitochondrial proteins, thereby controlling mitochondrial damage and mitophagy. Remarkably, since mitochondrial function has a crucial role in the pathogenesis of various diseases (e.g., cancer, atherosclerosis, Duchenne muscular dystrophy, diabetes complications, Alzheimer's disease, and hepatic steatosis), these effects might have important therapeutic implications. In this review, preclinical studies investigating the role of different natural compounds in the modulation of mitophagy will be discussed.

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“…Recent studies reported that curcumin could prevent cisplatin-induced AKI effectively [6]. Ortega-Dominguez et al showed that curcumin could protect cisplatin-induced AKI by preventing changes in mitochondrial bioenergy, ultrastructure, redox balance dynamics, and sirtuin-3 (SIRT3) expression levels [7]. Another study showed that curcumin reduced cisplatininduced renal toxicity by suppressing renal tubular cell apoptosis [8].…”

Section: Introductionmentioning

confidence: 99%

The renoprotective effect of curcumin against cisplatin-induced acute kidney injury in mice: involvement of miR-181a/PTEN axis

Huang

Yan

et al. 2020

Renal Failure

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Gong (2020) The renoprotective effect of curcumin against cisplatin-induced acute kidney injury in mice: involvement of miR-181a/PTEN axis, Renal Failure, 42:1, 350-357, ABSTRACT Background: Nephrotoxicity, especially acute kidney injury (AKI), is the main dose-limiting toxicity of cisplatin. Although recent studies showed that curcumin prevented cisplatin-induced AKI effectively, further studies to understand the mechanism are required. Methods: We established an AKI mouse model. Male C57BL/6 mice were assigned to three groups: saline group (control), cisplatin group (CP), and curcumin þ cisplatin group (CP þ Cur). The CP group received a single intraperitoneal (i.p.) injection of cisplatin, while the control group received saline. The CP þ Cur group received i.p. curcumin three days before cisplatin injection and curcumin administered for another three days until the day before euthanization. Renal injury was assessed by serological and histological analysis. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the phosphatase and tensin homolog (PTEN), and microRNA (miR)-181a expression in the renal tissues. Bioinformatics prediction and western blotting methods validated the targets of miR-181a in vitro. Results: Curcumin treatment alleviated cisplatin-induced nephrotoxicity as validated by the blood urea nitrogen (BUN) values, and histological analysis of kidneys. At the molecular level, curcumin treatment decreased miR-181a expression level, which was induced by cisplatin and restored the in vivo expression of PTEN, which was suppressed by cisplatin. We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells. Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.

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Curcumin prevents cisplatin-induced renal alterations in mitochondrial bioenergetics and dynamic

Cited by 106 publications

References 47 publications

Effective Nephroprotection Against Acute Kidney Injury with a Star-Shaped Polyglutamate-Curcuminoid Conjugate

Effective Nephroprotection Against Acute Kidney Injury with a Star-Shaped Polyglutamate-Curcuminoid Conjugate

Effects of Plant and Animal Natural Products on Mitophagy

The renoprotective effect of curcumin against cisplatin-induced acute kidney injury in mice: involvement of miR-181a/PTEN axis

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