Curcumin Attenuates Urinary Excretion of Albumin in Type II Diabetic Patients with Enhancing Nuclear Factor Erythroid-Derived 2-Like 2 (Nrf2) System and Repressing Inflammatory Signaling Efficacies

Yang, Haiyan; Xu, Wei; Zhou, Ziyu; Liu, J.; Li, X.; Chen, L.; Weng, Jianping; Zhong, Yu

doi:10.1055/s-0035-1545345

Cited by 91 publications

(73 citation statements)

References 28 publications

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“…Under physiological conditions, Nrf2 exists in the cytoplasm where it binds with Keap1 protein (28). When oxidative stress from external stimuli occurs, phosphorylation of Nrf2 separates it from the adapter protein Keap1 and transfers it into the cell nucleus to combine with the promoter sequence to regulate its downstream genes (29). The Nrf2 anti-apoptotic pathway has multiple functions relating to protection against anti-oxidative stress, regulation of inflammatory injury and relief from calcium overloading (30).…”

Section: Discussionmentioning

confidence: 99%

Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Cui

Song

Shi

2017

Experimental and Therapeutic Medicine

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Curcumin has previously demonstrated anti-inflammatory, anti-infective and immuno-suppressive effects. In the present study, whether the attenuating effects of curcumin against hypoxic-ischemic brain injury in neonatal rats are mediated via nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was investigated. A model of hypoxic-ischemic brain injury was created using 1-week-old Sprague Dawley rats (weight, 52±1 g). The model rats were treated with 150 mg/kg curcumin by gavage for 3 days. Malondialdehyde levels, and superoxide dismutase and caspase-3 activities were assayed using commercial kits and western blot analysis was used to measure inducible nitric oxide synthase (iNOS), Nrf2 and HO-1 expression levels. Treatment with curcumin effectively reduced the brain injury score, increased myelin basic protein (MBP) expression and increased the quantity of neuronal cells in neonatal rats with hypoxic-ischemic brain injury. Furthermore, treatment with curcumin significantly attenuated the changes in SOD activity and MDA levels and suppressed the iNOS protein expression induced in neonatal rats by hypoxic-ischemic brain injury. Treatment with curcumin significantly increased Nrf2 and HO-1 expression in the neonatal rats with hypoxic-ischemic brain injury. The present study indicated that curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through the induction of Nrf2 and HO-1.

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Section: Discussionmentioning

confidence: 99%

Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Cui

Song

Shi

2017

Experimental and Therapeutic Medicine

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“…Curcumin is also involved in osteoclastogenesis via signalosome-associated kinases and the proteasome-ubiquitin system. Studies by Yang et al [7] and Jung et al [10] found that curcumin inhibited inflammatory activity via activation of enhancing nuclear factor erythroid-derived 2-like 2 in patients with type 2 diabetes and murine macrophages, respectively. Furthermore, curcumin is known as "the king of spices" on account of its epigenetic regulatory properties with regard to preventing cancer and neurologic and inflammatory diseases, such as breast carcinoma, osteogenic sarcoma, osteoarthritis, and neurocognitive disorders [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Inhibits Polyethylene-Induced Osteolysis via Repressing NF-κB Signaling Pathway Activation

An¹,

Han²,

Hu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Aseptic loosening is a common reason for failed artificial hip replacement after total hip arthroplasty. Aseptic loosening is mostly the result of wear debris that causes osteolysis and weakens the structures that support the prosthesis. Wear debris plays a crucial role in osteolysis during the loosening process, and polyethylene (PE) particles are found as wear debris more frequently than any other type of particle. In the absence of effective therapeutic agents, osteolysis has been hard to treat. Previous studies have demonstrated that curcumin influences signalosome-associated kinases and the proteasome-ubiquitin system during osteoclastogenesis. The aims of this study were to explore the anti-osteolysis effect of curcumin and if possible to identify the signaling pathway involved in a model of PE-induced osteolysis. Methods: Differentiation of osteoclasts was induced in vitro by PE particles in RAW264.7 (monocyte/macrophage) cells and in vivo by calvarial and air pouch models of osteolysis established by PE stimulation in mice. We performed a set of TRAP staining, realtime polymerase chain reaction (PCR), and Western blot experiments to evaluate the anti-osteolytic effect of curcumin by comparing specimens that were exposed and not exposed to curcumin. Results: Curcumin had a promising inhibitory effect on osteolysis induced by wear debris and suppressed the RANK/c-Fos/NFATc1 signaling pathway. Conclusion: Curcumin can prevent PE-induced osteolysis and bone loss. An inhibitory effect on the RANK/c-Fos/NFATc1 signaling pathway may explain the anti-osteolysis activity of curcumin.

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“…These effects of curcumin on Nrf2 pathway have also been seen in human clinical trials involving patients with type 2 diabetes mellitus who each received an oral dose of curcumin of 500 mg/day for 15-30 days. This treatment induced an upregulation of Nrf2 in lymphocytes that controls other proteins, such as NAD(P)H quinone dehydrogenase 1 (NQO1), reduces inflammatory markers, and reduces plasma MDA levels [60]. In addition, curcumin supplementation of the diet increases NO bioavailability and inhibits the expression of pro-oxidative NADPH oxidase 2 (NOX-2) enzyme in rats [61].…”

Section: Introductionmentioning

confidence: 99%

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

et al. 2020

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Atherosclerosis is the main process behind cardiovascular diseases (CVD), maladies which continue to be responsible for up to 70% of death worldwide. Despite the ongoing development of new and potent drugs, their incomplete efficacy, partial intolerance and numerous side effects make the search for new alternatives worthwhile. The focus of the scientific world turned to the potential of natural active compounds to prevent and treat CVD. Essential for effective prevention or treatment based on phytochemicals is to know their mechanisms of action according to their bioavailability and dosage. The present review is focused on the latest data about phenolic compounds and aims to collect and correlate the reliable existing knowledge concerning their molecular mechanisms of action to counteract important risk factors that contribute to the initiation and development of atherosclerosis: dyslipidemia, and oxidative and inflammatory-stress. The selection of phenolic compounds was made to prove their multiple benefic effects and endorse them as CVD remedies, complementary to allopathic drugs. The review also highlights some aspects that still need clear scientific explanations and draws up some new molecular approaches to validate phenolic compounds for CVD complementary therapy in the near future.In the last decade the scientific researchers turned their attention to phytochemicals, as effective, safe and low-cost natural bioactive compounds for CVD treatment.Dyslipidemia consists of increased blood concentrations of total cholesterol (TC), low density lipoproteins-cholesterol (LDL-C) and/or triglycerides (TG), and decreased high density lipoproteins-cholesterol (HDL-C) [6]. The lipid metabolism is complex and the candidate mechanisms that could generate dyslipidemia include: (i) excessive dietary lipid absorption in the small intestine; (ii) packing of exogenous lipids with cholesterol and fatty acids produced de novo in the liver and their secretion as very low density lipoproteins (VLDL); (iii) hydrolysis of TG from VLDL by lipases and their conversion into LDL, which are taken up by the peripheral tissues through LDL receptor (LDL-R) and scavenger receptors; (iv) diminished production of HDL by the liver and small intestine, thereby decreasing reverse cholesterol transport (RCT) from the peripheral tissues to the liver; (v) lowered excess cholesterol excretion from the liver into gallbladder or to the intestinal lumen through the ATP-binding cassette G5 and G8 transporters (ABCG5/G8) that facilitate trans-intestinal cholesterol efflux (TICE). Dyslipidemia is associated with the accumulation of LDL in the sub-endothelium of the artery wall. At this site, LDL undergoes oxidative modifications (oxLDL) that trigger inflammatory responses, and is taken up by the monocyte-derived macrophages infiltrated in the sub-endothelium which thus become lipid-loaded foam cells, the hallmark of atheroma development [7]. Until now, the most effective lipid-lowering treatment for hyperlipidemic patients was the statin therapy. But recen...

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Curcumin Attenuates Urinary Excretion of Albumin in Type II Diabetic Patients with Enhancing Nuclear Factor Erythroid-Derived 2-Like 2 (Nrf2) System and Repressing Inflammatory Signaling Efficacies

Cited by 91 publications

References 28 publications

Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Curcumin attenuates hypoxic-ischemic brain injury in neonatal rats through induction of nuclear factor erythroid-2-related factor 2 and heme oxygenase-1

Curcumin Inhibits Polyethylene-Induced Osteolysis via Repressing NF-κB Signaling Pathway Activation

Phenolic Compounds Exerting Lipid-Regulatory, Anti-Inflammatory and Epigenetic Effects as Complementary Treatments in Cardiovascular Diseases

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