The synthesis of sulforaphane analogues and their protection effect against cisplatin induced cytotoxicity in kidney cells

Kim, Taejung; Kim, Youngjoo; Han, Im-Ho; Lee, Dahae; Ham, Jungyeob; Kang, Ki Sung; Lee, Jae Woo

doi:10.1016/j.bmcl.2014.11.014

Cited by 34 publications

(20 citation statements)

References 50 publications

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“…In our experiments using mouse models of sepsisand IRI-induced AKI, we observed that the beneficial effects of resveratrol and ethyl pyruvate are attributed to their ability to scavenge ROS and prevent release of proinflammatory HMGB1 in the circulation (242). The renoprotective effects of resveratrol and sulforaphane (an isothiocyanate that is found in vegetables) are also mediated by their ability to upregulate NRF-2 signaling and protect mitochondrial function (149,153,200,279). The upregulation of NRF-2 results in downstream stimulation of various antioxidants, including glutathione, thioredoxin, SOD, and catalase.…”

Section: Naturally Occurring Antioxidantsmentioning

confidence: 81%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

559

513

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Significance: A common link between all forms of acute and chronic kidney injuries, regardless of species, is enhanced generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during injury/ disease progression. While low levels of ROS and RNS are required for prosurvival signaling, cell proliferation and growth, and vasoreactivity regulation, an imbalance of ROS and RNS generation and elimination leads to inflammation, cell death, tissue damage, and disease/injury progression. Recent Advances: Many aspects of renal oxidative stress still require investigation, including clarification of the mechanisms which prompt ROS/ RNS generation and subsequent renal damage. However, we currently have a basic understanding of the major features of oxidative stress pathology and its link to kidney injury/disease, which this review summarizes. Critical Issues: The review summarizes the critical sources of oxidative stress in the kidney during injury/ disease, including generation of ROS and RNS from mitochondria, NADPH oxidase, and inducible nitric oxide synthase. The review next summarizes the renal antioxidant systems that protect against oxidative stress, including superoxide dismutase and catalase, the glutathione and thioredoxin systems, and others. Next, we describe how oxidative stress affects kidney function and promotes damage in every nephron segment, including the renal vessels, glomeruli, and tubules. Future Directions: Despite the limited success associated with the application of antioxidants for treatment of kidney injury/disease thus far, preventing the generation and accumulation of ROS and RNS provides an ideal target for potential therapeutic treatments. The review discusses the shortcomings of antioxidant treatments previously used and the potential promise of new ones.

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Section: Naturally Occurring Antioxidantsmentioning

confidence: 81%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

559

513

View full text Add to dashboard Cite

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“…However, due to the reactivity of the phenolic hydroxyl, the method used for the preparation of isothiocyanate 13a afforded 14a in rather low yield (26%). Thus, a method previously reported for preparation of isothiocyanate 14 11 was used to prepare 14a; treatment of 33a with of CS 2 followed by (t-Boc) 2 O yielded 14a in reasonable yield (63% yield from 32a). Isothiocyanate 14 11 and dithiocarbamate 16 12 were previously synthesized from commercially available tyramine (33), but the corresponding tetradeuterated compounds have not been reported previously.…”

Section: Resultsmentioning

confidence: 99%

“…The [2,3,5,6-D 4 ]nitro compound 30a was reduced to [2,3,5,6-D 4 ]-4-aminophenylacetonitrile (31a), which was then converted to [2,3,5,6-D 4 ]-4hydroxyphenylacetonitrile (32a) via diazotization and subsequent Cu(I)-catalyzed hydrolysis. Thus, a method previously reported for preparation of isothiocyanate 14 11 was used to prepare 14a; treatment of 33a with of CS 2 followed by (t-Boc) 2 O yielded 14a in reasonable yield (63% yield from 32a). However, due to the reactivity of the phenolic hydroxyl, the method used for the preparation of isothiocyanate 13a afforded 14a in rather low yield (26%).…”

Section: Synthesis Of Isothiocyanates Dithiocarbamates and Nasturmentioning

confidence: 99%

“…10 Next, reduction of nitrile 32a by using ZrCl 4 and NaBH 4 afforded [2,3,5,6-D 4 ]tyramine (33a), 7 which was used for the synthesis of [2,3,5,6-D 4 ]dithiocarbamate 16a, as described for compound 1a. Isothiocyanate 14 11 and dithiocarbamate 16 12 were previously synthesized from commercially available tyramine (33), but the corresponding tetradeuterated compounds have not been reported previously. Thus, a method previously reported for preparation of isothiocyanate 14 11 was used to prepare 14a; treatment of 33a with of CS 2 followed by (t-Boc) 2 O yielded 14a in reasonable yield (63% yield from 32a).…”

Section: Synthesis Of Isothiocyanates Dithiocarbamates and Nasturmentioning

confidence: 99%

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Synthesis of stable isotope‐labeled nasturlexins and potential precursors to probe biosynthetic pathways of cruciferous phytoalexins

Pedras

2018

Labelled Comp Radiopharmac

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The syntheses of perdeuterated phytoalexins nasturlexins A and C, and putative biosynthetic precursors, including phenylethyl isothiocyanates and phenylethyl dithiocarbamates, using commercially available [2,3,4,5,6-D ]phenylalanine, [2,3,4,5,6-D ]nitrobenzene, and [2,3,4,5,6-D ]benzaldehyde are described. In addition, application of an efficient deuterium-hydrogen exchange transformation to nonlabeled starting materials allowed access to new deuterated compounds, including 3-hydroxyphenylethyl glucosinolate.

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“…Recent studies have suggested that nephrotoxicity is dependent on DNA damage related to apoptosis [6]. In addition, dysregulation of MAPK signaling pathways has been demonstrated in acute and chronic kidney disease induced by cisplatin [7].…”

Section: Introductionmentioning

confidence: 99%

Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells

Lee

Kang

2017

Journal of Ginseng Research

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BackgroundGinsenosides are active components of Panax ginseng that exert various health benefits including kidney protection effect. The medicinal activity of ginsenosides can be enhanced by modulating their stereospecificity by heat processing. Ginsenosides Rk2 and Rh3 represent positional isomers of the double bond at C-20(21) or C-20(22).MethodsThe present study investigated the kidney-protective effects of ginsenosides Rk2 and Rh3 against cisplatin, a platinum based anticancer drug, induced apoptotic damage in renal proximal LLC-PK1 cells.ResultsAs a result, ginsenoside Rh3 shows a stronger protective effect than that shown by Rk2. Cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), p38, and cleaved caspase-3 decreased after cotreatment with ginsenoside Rh3. The increase in the percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment also significantly reduced after cotreatment with ginsenoside Rh3.ConclusionThese results demonstrate that inhibition of the JNK and ERK mitogen-activated protein kinase signaling cascade plays a critical role in mediating the renoprotective effect of ginsenoside Rh3.

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The synthesis of sulforaphane analogues and their protection effect against cisplatin induced cytotoxicity in kidney cells

Cited by 34 publications

References 50 publications

Oxidant Mechanisms in Renal Injury and Disease

Oxidant Mechanisms in Renal Injury and Disease

Synthesis of stable isotope‐labeled nasturlexins and potential precursors to probe biosynthetic pathways of cruciferous phytoalexins

Protective effect of ginsenoside Rh3 against anticancer drug-induced apoptosis in LLC-PK1 kidney cells

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