The Antioxidant 3H-1,2-Dithiole-3-Thione Potentiates Advanced Glycation End-Product-Induced Oxidative Stress in SH-SY5Y Cells

Pazdro, Robert; Burgess, John

doi:10.1155/2012/137607

Cited by 21 publications

(15 citation statements)

References 49 publications

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“…NQO1 is a cytosolic antioxidant flavoprotein that catalyzes the reduction of quinones to hydroquinones and detoxifies by utilizing NADH as an electron donor, which consequently increases intracellular NAD + levels 74) . Additionally, there is evidence that NQO1 has a role in other biological effects, including anti-inflammatory processes, scavenging of superoxide anion radicals, and stabilization of p53 and other tumor-suppressor proteins 75 , 76 , 77) . β-Lapachone (3, 4-dihydro-2, 2-dimethyl-2H-naphto [1, 2-b] pyran-5, 6-dione) is a well-known substrate of NQO1 78) .…”

Section: Protection Against Cisplatin-induced Renal Dysfunctionmentioning

confidence: 99%

Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies

Kim

Shen

et al. 2014

Electrolyte Blood Press

175

131

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Cisplatin is one of the most widely used and highly effective drug for the treatment of various solid tumors; however, it has dose-dependent side effects on the kidney, cochlear, and nerves. Nephrotoxicity is the most well-known and clinically important toxicity. Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage, and inflammatory responses, are closely associated with cisplatin-induced nephrotoxicity. Even though the establishment of cisplatin-induced nephrotoxicity can be alleviated by diuretics and pre-hydration of patients, the prevalence of cisplatin nephrotoxicity is still high, occurring in approximately one-third of patients who have undergone cisplatin therapy. Therefore it is imperative to develop treatments that will ameliorate cisplatin-nephrotoxicity. In this review, we discuss the mechanisms of cisplatin-induced renal toxicity and the new strategies for protecting the kidneys from the toxic effects without lowering the tumoricidal activity.

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Section: Protection Against Cisplatin-induced Renal Dysfunctionmentioning

confidence: 99%

Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies

Kim

Shen

et al. 2014

Electrolyte Blood Press

175

131

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“…However, apart from their role as intracellular signaling molecules, ROS exert cytotoxic effects such as peroxidation of lipids and phospholipids [7] , and oxidative damage to proteins and DNA [8] . Therefore, cells have several protective mechanisms against these oxidative stressors [9] , [10] , [11] most of which induce cytoprotective enzymes [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] and ROS scavenging. Taken together, it is thought that cytoprotective mechanisms are attenuated during osteoclastogenesis to intensify intracellular ROS signaling.…”

Section: Introductionmentioning

confidence: 99%

Molecular regulatory mechanisms of osteoclastogenesis through cytoprotective enzymes

et al. 2016

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It has been reported that reactive oxygen species (ROS), such as hydrogen peroxide and superoxide, take part in osteoclast differentiation as intra-cellular signaling molecules. The current assumed signaling cascade from RANK to ROS production is RANK, TRAF6, Rac1, and then Nox. The target molecules of ROS in RANKL signaling remain unclear; however, several reports support the theory that NF-κB signaling could be the crucial downstream signaling molecule of RANKL-mediated ROS signaling. Furthermore, ROS exert cytotoxic effects such as peroxidation of lipids and phospholipids and oxidative damage to proteins and DNA. Therefore, cells have several protective mechanisms against oxidative stressors that mainly induce cytoprotective enzymes and ROS scavenging. Three well-known mechanisms regulate cytoprotective enzymes including Nrf2-, FOXO-, and sirtuin-dependent mechanisms. Several reports have indicated a crosslink between FOXO- and sirtuin-dependent regulatory mechanisms. The agonists against the regulatory mechanisms are reported to induce these cytoprotective enzymes successfully. Some of them inhibit osteoclast differentiation and bone destruction via attenuation of intracellular ROS signaling. In this review article, we discuss the above topics and summarize the current information available on the relationship between cytoprotective enzymes and osteoclastogenesis.

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“…Advanced glycation end products are colocalized in amyloid plaques in the brains of AD patients [3–5] . Many experimental studies indicate that the interaction between AGEs and RAGE elicits intracellular oxidative stress, proinflammatory apoptosis, and oxidative stress responses, which lead to nerve cell damage [6,7] . These signal transduction pathways may be associated with RAGE/nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) pathway [8] .…”

Section: Introductionmentioning

confidence: 99%

Ginseng improves cognitive deficit via the RAGE/NF-κB pathway in advanced glycation end product-induced rats

Tan

Zhao

et al. 2015

Journal of Ginseng Research

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BackgroundGinseng, the root of Panax ginseng (PG), is used widely as a herbal medicine to prevent and treat various diseases. Panax ginseng has pharmacological effects on neurodegenerative diseases such as Alzheimer's disease (AD). The present study evaluated the neuroprotective effects of PG and its possible neuroprotective mechanisms in advanced glycation end product (AGE)-induced AD in a rat model.MethodsAdvanced glycation end products were injected bilaterally into the CA3 region of the rats' brains. The Morris water maze test and step-down type passive avoidance test were performed to evaluate their memory and cognitive abilities. The oxidation indexes in the hippocampus were detected. Immunohistochemistry was conducted to visualize the receptors for advanced glycation end products (RAGEs) and nuclear factor-kappa-light-chain-enhancer of activated B cell (NF-κB).ResultsBehavioral results showed that PG (1 g/kg, 0.5 g/kg, and 0.25 g/kg) significantly shortened the escape latency, remarkably increased the number of crossing times, significantly decreased the number of errors, and prolonged the latency in rats with AGE-induced AD. Panax ginseng also significantly reduced the malondialdehyde level, increased the glutathione content, and increased superoxide dismutase activity in the hippocampus. Panax ginseng significantly decreased the expression of RAGE and NF-κB. The blockade of anti-RAGE antibody could significantly reduce AGE-induced impairments and regulate these expressions.ConclusionOur results demonstrated that PG significantly inhibits AGE-induced memory impairment and attenuates Alzheimer-like pathophysiological changes. These neuroprotective effects of PG may be associated with the RAGE/NF-κB pathway. Our results provided the experimental basis for applying PG in preventing and treating AD.

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The Antioxidant 3H-1,2-Dithiole-3-Thione Potentiates Advanced Glycation End-Product-Induced Oxidative Stress in SH-SY5Y Cells

Cited by 21 publications

References 49 publications

Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies

Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies

Molecular regulatory mechanisms of osteoclastogenesis through cytoprotective enzymes

Ginseng improves cognitive deficit via the RAGE/NF-κB pathway in advanced glycation end product-induced rats

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