Elevated cAMP level attenuates 2-deoxy-d-ribose-induced oxidative damage in pancreatic β-cells

Koh, Gwanpyo; Suh, Kwang Sik; Chon, Suk; Oh, Seungjoon; Woo, Jeong-Taek; Kim, Sung-Woon; Kim, Jin-Woo; Kim, Young-Seol

doi:10.1016/j.abb.2005.03.018

Cited by 44 publications

(53 citation statements)

References 53 publications

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“…We previously reported that dRib treatment gave rise to oxidative stress and apoptosis in HIT-T15 cells 4,5) and that the restoration of intracellular GSH levels was a prerequisite for protecting the cells against dRib-induced oxidative damage. However, we still do not understand the mechanism of action of dRib.…”

Section: Discussionmentioning

confidence: 99%

“…4) HIT-T15 cells were plated in 6-well culture plates at a density of 5×10 5 per well. The cells were stimulated with 50 mM dRib and LA for only 6 h because extensive cell death could interfere with ROS measurements.…”

Section: )mentioning

confidence: 99%

“…HIT-T15 cells were cultured in 6-well culture plates at a density of 5×10 5 per well. The cells were preincubated with LA for 30 min and then cultured with 35 mM dRib for 6 h. Cells were washed with ice-cold DPBS and sonicated, followed by centrifugation at 10000×g for 15 min.…”

Section: )mentioning

confidence: 99%

“…4,9) Briefly, HIT-T15 cells were cultured in 6-well plates at a density of 5×10 5 per well. The cells were stimulated with 50 mM dRib and LA for 24 h. The stained cells were analyzed using a fluorescenceactivated cell sorter (FACSCalibur, BD Bioscience, San Jose, CA, U.S.A.) and quadrant data were calculated with CellQuest software (BD Bioscience).…”

Section: )mentioning

confidence: 99%

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Alpha-Lipoic Acid Treatment Reverses 2-Deoxy-D-ribose-Induced Oxidative Damage and Suppression of Insulin Expression in Pancreatic Beta-Cells

Koh

Yang

Kim³

et al. 2013

Biological & Pharmaceutical Bulletin

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We investigated whether α-lipoic acid (LA) could prevent 2-deoxy-D-ribose (dRib)-induced oxidative damage and suppression of insulin expression in pancreatic β-cells. Stimulation with 50 mM dRib elevated cytotoxicity, apoptosis and intracellular reactive oxygen species (ROS) levels in HIT-T15 cells, but pretreatment with LA significantly reversed the dRib-induced changes. LA directly scavenged hydroxyl radicals generated by a Fenton reaction. Intracellular reduced glutathione (GSH) and oxidized glutathione (GSSG) were depleted by stimulation with dRib but levels were restored by addition of LA to HIT-T15 cells. However, the GSH/GSSG ratio was unchanged by LA treatment. In rat islets, stimulation with 10 mM dRib for 6 h suppressed expression of insulin and pancreatic and duodenal homeobox 1 mRNA and decreased insulin content, but these were dose-dependently reversed when LA was added. Treatment with L-buthioninesulfoximine, an inhibitor of intracellular glutathione biosynthesis, completely abolished the protective effects of LA on dRib-mediated glutathione depletion and cytotoxicity in HIT-T15 cells. In summary, LA reversed the dRib-induced oxidative damage and suppression of insulin expression in β-cells. Enhanced intracellular total glutathione production, rather than the scavenging of ROS, is possibly the mechanism for the protective effect of LA.

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Section: Discussionmentioning

confidence: 99%

Section: )mentioning

confidence: 99%

Section: )mentioning

confidence: 99%

Section: )mentioning

confidence: 99%

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Alpha-Lipoic Acid Treatment Reverses 2-Deoxy-D-ribose-Induced Oxidative Damage and Suppression of Insulin Expression in Pancreatic Beta-Cells

Koh

Yang

Kim³

et al. 2013

Biological & Pharmaceutical Bulletin

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“…The various forms of executive dysfunction, visuospatial impairment, memory impairment, and attention defi cits that occur in PD can render patients less able to accomplish familiar tasks or make them feel overwhelmed in situations that were not previously challenging [421,422]. The presence of a mood disorder which can precede, accompany or follow cognitive changes may also confound assessment of cognitive impairment and intensify defi cits [142,177].…”

Section: Fsk and Cognitive Dysfunctionsmentioning

confidence: 99%

Restoration of Mitochondrial Dysfunction in 6-Hydroxydopamine Induced Parkinson’s disease: a Complete Review

Mehan¹,

Kaur²,

Dudi³

et al. 2017

Open J Parkinsons Dis Treatm

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Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by neuronal cell death in the specifi c brain region like basal ganglia, cerebral cortex and hippocampus. Symptoms associated with PD patients are rigidity, akathesia, tremor, postural imbalance, cognitive and memory dysfunctions. Pathological hallmarks are dopaminergic neuronal degeneration, neuro-infl ammation, oxidative stress, free radical generation. In the typical Parkinson's disease model, 6-Hydroxydopamine (6-OHDA) is delivered unilaterally by stereotactic injection into the SNc (substantia nigra pars-compacta) or the striatum mimics the PD symptoms. In addition, it has been shown that 6-OHDA is toxic to complex I & IV of the mitochondrial respiratory chain, leading to subsequent respiratory inhibition and further processed ATP depletion, oxidative stress and neuro-infl ammation. Forskolin (FSK), a diterpene natural plant phytochemical obtained from (Coleus Forskohli), a potent direct activator of adenyl cyclase (AC) enzyme which further activates cAMP/PK A /CREB pathway. FSK mediated activation of AC/cAMP/PK A / CREB pathway is responsible for various neuroprotective mechanisms Based on important and versatile role of FSK, the present study has been designed to investigate the role of cAMP mediated CREB activation in 6-hydroxydopamine induced mitochondrial associated neurotoxicity in rats. Further the studies are extended to understand the disease pathogenesis and to investigate and discuss the various possible central mechanisms involved in the effect of such targets using behavioral paradigm and biochemical markers of neurodegeneration.

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Kaempferol protects HIT‐T15 pancreatic beta cells from 2‐deoxy‐D‐ribose‐induced oxidative damage

Lee

Suh

Choi

et al. 2009

Phytotherapy Research

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During the progression of Type 2 diabetes, glucose toxicity is likely to contribute importantly to progressive beta cell failure. Oxidative stress is an important aspect of glucose toxicity in pancreatic beta cells, and reducing sugars, such as 2-deoxy-D-ribose (dRib), produce reactive oxygen species. Furthermore, many of the biological properties of flavonoids are likely to be related to their antioxidant and free-radical scavenging abilities. Accordingly, in the present study, we investigated whether kaempferol (a flavonol) protects beta cells from dRib-induced oxidative damage. HIT-T15 cells were cultured with various concentrations of dRib for 24h. Cell survivals, amounts of reactive oxygen species (ROS) generated, apoptosis, and lipid peroxidation were measured. dRib was found to dose-dependently reduce cell survival and to markedly increase intracellular ROS levels, apoptosis, and lipid peroxidation. However, kaempferol (10 microM) suppressed dRib (20 mM) induced intracellular ROS, apoptosis, and lipid peroxidation. So, we demonstrate that kaempferol reduces dRib-mediated beta cell damage interfering with ROS metabolism and protective effects against lipid peroxidation. Our findings indicate that kaempferol protects HIT-T15 cells from dRib-induced associated oxidative damage.

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Elevated cAMP level attenuates 2-deoxy-d-ribose-induced oxidative damage in pancreatic β-cells

Cited by 44 publications

References 53 publications

Alpha-Lipoic Acid Treatment Reverses 2-Deoxy-D-ribose-Induced Oxidative Damage and Suppression of Insulin Expression in Pancreatic Beta-Cells

Alpha-Lipoic Acid Treatment Reverses 2-Deoxy-D-ribose-Induced Oxidative Damage and Suppression of Insulin Expression in Pancreatic Beta-Cells

Restoration of Mitochondrial Dysfunction in 6-Hydroxydopamine Induced Parkinson’s disease: a Complete Review

Kaempferol protects HIT‐T15 pancreatic beta cells from 2‐deoxy‐D‐ribose‐induced oxidative damage

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