Role of curcumin in the treatment of acute kidney injury: research challenges and opportunities

Cai, Yuanqiang; Huang, Chaoming; Zhou, Mengyu; Xu, Shiqi; Xie, Yongwan; Gao, Shuhan; Yang, Yantianyu; Deng, Zirong; Zhang, Libei; Shu, Jicheng; Yan, Tingdong; Wan, Chunpeng

doi:10.1016/j.phymed.2022.154306

Cited by 28 publications

(16 citation statements)

References 103 publications

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“…The onset is due to a lack of righteousness, exogenous damp-heat toxins, or drug poisoning. AKI caused by cisplatin is due to a lack of vital qi caused by drug poisoning ( Li et al, 2019 ; Liu et al, 2021 ; Cai et al, 2022 ). Currently, clinical drugs are lacking for treating renal injury induced by cisplatin ( Holditch et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Network pharmacology, molecular docking, and experimental verification reveal the mechanism of San-Huang decoction in treating acute kidney injury

Liu

Li²,

Lao³

et al. 2023

Front. Pharmacol.

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Background: Cisplatin is an effective anti-tumor drug. However, its usage is constrained by side effects such as nephron toxicity. Cisplatin-induced acute kidney injury (AKI) appears in approximately 20%–30% of cases. Hence, finding an effective protective strategy is necessary. San-Huang decoction (SHD) is a Chinese herbal decoction with good efficacy in treating chronic kidney disease (CKD). Nevertheless, the mechanism of SHD on AKI remains unclear. Consequently, we proposed to explore the potential mechanism of SHD against cisplatin-induced AKI.Methods: Active compounds, core target proteins, and associated signaling pathways of SHD were predicted through network pharmacology. Then confirmed by molecular docking. In vivo experiment, Cisplatin + SHD group was treated with SHD (6.5 g/kg/day) for 6 days before building the model. An AKI model was established with a single intraperitoneal injection of cisplatin at 20 mg/kg. After 72 h of cisplatin injection, all mice were sacrificed to collect blood and kidney tissues for verification of network pharmacology analysis.Results: We found that calycosin, rhein, and ginsenoside Rh2 may be SHD’s primary active compounds in treating cisplatin-induced AKI, and AKT, TNF-α, IL-6, IL-1β, caspase-3, and MMP9 are the core target proteins. The relationship between the compound and target protein was further confirmed by molecular docking. The Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses predicted that SHD has an anti-inflammatory role through the TNF and IL-17 signaling pathway. Moreover, Western blot and immunohistochemistry validated the potential molecular mechanisms of SHD, predicted from network pharmacology analysis. The mechanism of cisplatin-induced AKI involves apoptosis and inflammation. In apoptosis, Caspase-3, caspase-8, caspase-9, and Bax proteins were down-regulated, while Bcl-2 was up-regulated by SHD. The differential expression of MMP protein is involved in the pathological process of AKI. MMP9 protects from glomerular tubule damage. MMP9 and PI3K/AKT anti-apoptosis pathway were up-regulated by SHD. In addition, we discovered that SHD alleviated AKI by inhibiting the NF-κB signaling pathway.Conclusion: SHD plays a critical role in anti-inflammation and anti-apoptosis via inhibiting the NF-κB signaling pathway and activating PI3K/AKT anti-apoptosis pathway, indicating that SHD is a candidate herbal drug for further investigation in treating cisplatin-induced AKI.

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Section: Introductionmentioning

confidence: 99%

Network pharmacology, molecular docking, and experimental verification reveal the mechanism of San-Huang decoction in treating acute kidney injury

Liu

Li²,

Lao³

et al. 2023

Front. Pharmacol.

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“…Curcumin also prevented renal tubular oxidative damage by reducing ROS production. Furthermore, curcumin restored mitochondrial homeostasis by regulating OPA1, modulating DRP1 expression, and inhibiting caspase-3 activation [ 44 ]. Together, all results show that even with incomplete knowledge of the mechanism of action of curcumin for the modulation of inflammation, we can predict its beneficial effects on the outcome of mortality in sepsis.…”

Section: Discussionmentioning

confidence: 99%

Impacts of Curcumin Treatment on Experimental Sepsis: A Systematic Review

Vieira

Caetano

Carvalho

et al. 2023

Oxidative Medicine and Cellular Longevity

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Background and Aims. Sepsis is defined as a life-threatening organ dysfunction due to a dysregulated host immune response to an infection. Curcumin is a yellow polyphenol derived from the rhizome of Curcuma longa with anti-inflammatory and antioxidant properties scientifically proven, a condition that allowed its use as a tool in the treatment of sepsis. Thus, the purpose of this article was to systematically review the evidence on the impact of curcumin’s anti-inflammatory effect on experimental sepsis. Methods. For this, the PubMed, MEDLINE, EMBASE, Scopus, Web of Science, and LILACS databases were used, and the research was not limited to a specific publication period. Only original articles in English using in vivo experimental models (rats or mice) of sepsis induction performed by administration of lipopolysaccharide (LPS) or cecal ligation and perforation surgery (CLP) were included in the study. Studies using curcumin in dry extract or with a high degree of purity were included. At initial screening, 546 articles were selected, and of these, 223 were eligible for primary evaluation. Finally, 12 articles with full text met all inclusion criteria. Our results showed that curcumin may inhibit sepsis-induced complications such as brain, heart, liver, lungs, and kidney damage. Curcumin can inhibit inflammatory factors, prevent oxidative stress, and regulate immune responses in sepsis. Additionally, curcumin increased significantly the survival rates after experimental sepsis in several studies. The modulation of the immune response and mortality by curcumin reinforces its protective effect on sepsis and indicates a potential therapeutic tool for the treatment of sepsis.

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“…Hui et al found that resveratrol alleviates excessive mitochondrial fission and promotes mitochondrial fusion in TGF-β1-treated mesangial cells ( Li et al, 2021b ). Curcumin can also reverse mitochondrial fragmentation in renal TECs via inhibiting mitochondrial fission and promoting mitochondrial fusion in cisplatin-induced kidney injury ( Ortega-Domínguez et al, 2017 ; Cai et al, 2022 ).…”

Section: Natural Products For Regulating Mitochondrial Functionmentioning

confidence: 99%

Natural products for kidney disease treatment: Focus on targeting mitochondrial dysfunction

2023

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The patients with kidney diseases are increasing rapidly all over the world. With the rich abundance of mitochondria, kidney is an organ with a high consumption of energy. Hence, renal failure is highly correlated with the breakup of mitochondrial homeostasis. However, the potential drugs targeting mitochondrial dysfunction are still in mystery. The natural products have the superiorities to explore the potential drugs regulating energy metabolism. However, their roles in targeting mitochondrial dysfunction in kidney diseases have not been extensively reviewed. Herein, we reviewed a series of natural products targeting mitochondrial oxidative stress, mitochondrial biogenesis, mitophagy, and mitochondrial dynamics. We found lots of them with great medicinal values in kidney disease. Our review provides a wide prospect for seeking the effective drugs targeting kidney diseases.

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Role of curcumin in the treatment of acute kidney injury: research challenges and opportunities

Cited by 28 publications

References 103 publications

Network pharmacology, molecular docking, and experimental verification reveal the mechanism of San-Huang decoction in treating acute kidney injury

Network pharmacology, molecular docking, and experimental verification reveal the mechanism of San-Huang decoction in treating acute kidney injury

Impacts of Curcumin Treatment on Experimental Sepsis: A Systematic Review

Natural products for kidney disease treatment: Focus on targeting mitochondrial dysfunction

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