Presenting a New Standard Drug Model for Turmeric and Its Prized Extract, Curcumin

Cavaleri, Franco

doi:10.1155/2018/5023429

Cited by 18 publications

(12 citation statements)

References 256 publications

(273 reference statements)

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“…Because TNF-α transcription is known to be controlled by NFκB, which, in turn, is activated following dissociation from phosphorylated IκKβ. Indeed, inhibition of IκB kinase (IκK) by curcumin, if occurring, would decrease NFκB transcriptional activity and TNF-α expression ( Cavaleri, 2018 ). The docking score of curcumin bound to IκKβ ( Table 2 and Figure 1D ) was more favorable than docking at AKT1 and Toll-like receptor 9.…”

Section: Resultsmentioning

confidence: 99%

“…On the basis of literature search Toll-like receptor 9, AKT 1–2, and IκKβ/NFκB were selected from the list of putative targets of curcumin, predicted by SwissTargetPrediction. In fact, previous experimental data showed that curcumin was able to modulate activity of these targets involved in inflammatory processes ( Leclercq et al, 2004 ; Youn et al, 2006 ; Jacot and Sherris, 2011 ; Soetikno et al, 2011 ; Chen et al, 2017 ; Fan et al, 2017 ; Cavaleri, 2018 ). Therefore, we predicted through molecular docking calculations the binding mode of curcumin as inhibitor of the Toll-like receptor 9, of PI3K/AKT, and of the IκKβ/NFκB signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

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Retinal Protection and Distribution of Curcumin in Vitro and in Vivo

et al. 2018

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Diabetic retinopathy (DR), a secondary complication of diabetes, is a leading cause of irreversible blindness accounting for 5% of world blindness cases in working age. Oxidative stress and inflammation are considered causes of DR. Curcumin, a product with anti-oxidant and anti-inflammatory properties, is currently proposed as oral supplementation therapy for retinal degenerative diseases, including DR. In this study we predicted the pharmacodynamic profile of curcumin through an in silico approach. Furthermore, we tested the anti-oxidant and anti-inflammatory activity of curcumin on human retinal pigmented epithelial cells exposed to oxidative stress, human retinal endothelial and human retinal pericytes (HRPCs) cultured with high glucose. Because currently marketed curcumin nutraceutical products have not been so far evaluated for their ocular bioavailability; we assessed retinal distribution of curcumin, following oral administration, in rabbit eye. Curcumin (10 μM) decreased significantly (p < 0.01) ROS concentration and TNF-α release in retinal pigmented epithelial cells and retinal endothelial cells, respectively. The same curcumin concentration significantly (p < 0.01) protected retinal pericytes from high glucose damage as assessed by cell viability and LDH release. Among the tested formulations, only that containing a hydrophilic carrier provided therapeutic levels of curcumin in rabbit retina. In conclusion, our data suggest that curcumin, when properly formulated, may be of value in clinical practice to manage retinal diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Retinal Protection and Distribution of Curcumin in Vitro and in Vivo

et al. 2018

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“…CUR has established anti-inflammatory properties, and is known to protect cells against hyperactivated immune system via diverse pathways. 21 CUR is a known inhibitor of NF-κB, a key regulator of inflammation, which inhibits the expression of interleukins, including IL-1, IL-2, and IL-6, as well as TNF-α, CXCL1, and CXCL8. 15,21 Our results indicated that CUR treatment mitigated OXAinduced hepatocellular injury by inhibiting the production of the pro-inflammatory cytokines CXCL1, CXCL2, and MCP-1.…”

Section: Discussionmentioning

confidence: 99%

“…21 CUR is a known inhibitor of NF-κB, a key regulator of inflammation, which inhibits the expression of interleukins, including IL-1, IL-2, and IL-6, as well as TNF-α, CXCL1, and CXCL8. 15,21 Our results indicated that CUR treatment mitigated OXAinduced hepatocellular injury by inhibiting the production of the pro-inflammatory cytokines CXCL1, CXCL2, and MCP-1. Therefore, in addition to the inhibition of oxidative stress, the protective effect of CUR also correlated with the inhibition of hepatic inflammatory.…”

Section: Discussionmentioning

confidence: 99%

“…1,15,16 Especially in terms of its hepatoprotective effects, increasing evidence demonstrates that CUR exerts protective effects against toxins such as carbon tetrachloride, 17 alcohol, 18 N-nitrosodiethylamine, 19 and arsenic, 20 and these effects are related to its antioxidant activity. 21 Several studies have suggested that CUR possibly acts through activating the Nrf2 signaling pathway, effectively protecting the liver from oxidative damage induced by toxicants. 20,22 Additionally, increasing data shows that CUR activates Nrf2, which further initiates the expression of a variety of antioxidant enzymes and Phase II drug-metabolizing enzymes, including HO-1 and NAD(P) H:quinine oxidoreductase 1 (NQO1), and finally protects various tissues and cells against oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

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<p>Curcumin Attenuates Oxaliplatin-Induced Liver Injury and Oxidative Stress by Activating the Nrf2 Pathway</p>

Lu¹,

Wu²,

Xiang³

et al. 2020

DDDT

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Purpose: Oxaliplatin (OXA)-induced liver injury is one of the main limiting factors affecting the efficacy of OXA-based chemotherapy in patients with colorectal liver metastases. In addition, oxidative stress is an important pathophysiological mechanism of OXAinduced liver injury. Therefore, dietary antioxidants may decrease or prevent hepatic toxicity in vivo and be beneficial to OXA-based chemotherapy. Methods: An experimental OXA-induced liver injury animal model was established, and the protective effects of curcumin (CUR) against OXA-induced liver injury were investigated. ELISA was used to determine the levels of MDA, SOD, CAT, and GSH in liver tissue. The effect of CUR treatment on the expression of cytokines and the Nrf2 pathway was determined by real-time PCR and Western blotting. Results: CUR treatment alleviated OXA-induced hepatic pathological damage and splenomegaly. The protective effect of CUR was demonstrated to be correlated with inhibition of oxidative stress, inflammation, and the coagulation system. Furthermore, Western blotting revealed that CUR treatment reverses the suppression of Nrf2 nuclear translocation and increases the expression of HO-1 and NOQ1 in mice with OXA-induced liver injury. Moreover, the Nrf2 activation and hepatoprotective effect of CUR were abolished by brusatol. Conclusion: Curcumin attenuates oxaliplatin-induced liver injury and oxidative stress by activating the Nrf2 pathway, which suggests that CUR may be potentially used in the prevention and treatment of OXA-induced liver injury.

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Ameliorative effect of curcumin on lead‐induced hematological and hepatorenal toxicity in a rat model

Abubakar

Mailafiya

Chiroma

et al. 2020

J Biochem & Molecular Tox

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Introduction Lead (Pb) is a ubiquitous toxic heavy metal that inflicts numerous clinical consequences on humans. Curcumin is the principal component of turmeric, which is reported to have antioxidative properties. This study aimed at evaluating the ameliorative effects of curcumin on Pb‐induced hepatorenal toxicity in a rat model. Methods Thirty‐six male Sprague‐Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and six rats each for the lead‐treated group (LTG) (50 mg/kg lead acetate [Pb acetate] for 4 weeks), recovery group (50 mg/kg Pb acetate for 4 weeks and left with no treatment for another 4 weeks), treatment group 1 (Cur100) (50 mg/kg Pb acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks), and treatment group 2 (Cur200) (50 mg/kg Pb acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks). All the experimental groups received oral treatments via orogastric‐tube on alternate days. Pb concentration in the liver and kidney of the rats were evaluated using inductive‐coupled plasma mass spectrometry techniques. Results Pb‐administered rats revealed significant alteration in oxidative status and increased Pb concentration in their liver and kidney with obvious reduction of hemogram and increased in leukogram as well as aberration in histological architecture of the liver and kidney. However, treatment with curcumin reduces the tissue Pb concentrations and ameliorates the above mention alterations. Conclusions The results in this study suggested that curcumin attenuates Pb‐induced hepatorenal toxicity via chelating activity and inhibition of oxidative stress.

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Presenting a New Standard Drug Model for Turmeric and Its Prized Extract, Curcumin

Cited by 18 publications

References 256 publications

Retinal Protection and Distribution of Curcumin in Vitro and in Vivo

Retinal Protection and Distribution of Curcumin in Vitro and in Vivo

<p>Curcumin Attenuates Oxaliplatin-Induced Liver Injury and Oxidative Stress by Activating the Nrf2 Pathway</p>

Ameliorative effect of curcumin on lead‐induced hematological and hepatorenal toxicity in a rat model

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