Involvement of caspase-8, -9, and -3 in high glucose-induced apoptosis in PC12 cells

Sharifi, Ali Mohammad; Eslami, Habib; Larijani, Bagher; Davoodi, Jamsheed

doi:10.1016/j.toxlet.2009.06.342

Cited by 8 publications

(8 citation statements)

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“…To ensure that there are no confounding effects imposed by high osmolarity, we also performed experiments in the presence of mannitol (100 mM for 24 hr) as osmotic control for high glucose, in accordance with reported studies (El‐Remessy, Abou‐Mohamed, Caldwell, & Caldwell, 2003; Fouda & Abdel‐Rahman, 2017; Sharifi, Eslami, Larijani, & Davoodi, 2009).…”

Section: Methodsmentioning

confidence: 89%

Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels

Fouda

Ghovanloo

Ruben

2020

British J Pharmacology

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Background and Purpose: Cardiovascular complications are the major cause of mortality in diabetic patients. However, the molecular mechanisms underlying diabetesassociated arrhythmias are unclear. We hypothesized that high glucose could adversely affect Na v 1.5, the major cardiac sodium channel isoform of the heart, at least partially via oxidative stress. We further hypothesized that cannabidiol (CBD), one of the main constituents of Cannabis sativa, through its effects on Na v 1.5, could protect against high glucose-elicited oxidative stress and cytotoxicity.Experimental Approach: To test these ideas, we used CHO cells transiently cotransfected with cDNA encoding human Na v 1.5 α-subunit under control and high glucose conditions (50 or 100 mM for 24 hr). Several experimental and computational techniques were used, including voltage clamp of heterologous expression systems, cell viability assays, fluorescence assays and action potential modelling.Key Results: High glucose evoked cell death associated with elevation in reactive oxygen species (ROS) right shifted the voltage dependence of conductance and steady-state fast inactivation, and increased persistent current leading to computational prolongation of action potential (hyperexcitability) which could result in long QT3 arrhythmia. CBD mitigated all the deleterious effects provoked by high glucose.Perfusion with lidocaine (a well-known sodium channel inhibitor with antioxidant effects) or co-incubation of Tempol (a well-known antioxidant) elicited protection, comparable to CBD, against the deleterious effects of high glucose.Conclusion and Implications: These findings suggest that, through its favourable antioxidant and sodium channel inhibitory effects, CBD may protect against high glucose-induced arrhythmia and cytotoxicity.

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Section: Methodsmentioning

confidence: 89%

Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels

Fouda

Ghovanloo

Ruben

2020

British J Pharmacology

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“…In an in vitro investigation, Sharifi and colleagues demonstrated that the suppression of apoptotic proteins by Z-VAD-FMK (as a caspase inhibitor) inhibits the cell toxicity induced by high glucose levels [26]. Joseph and Levine reported that caspases (as components of apoptosis signaling pathways) contribute to the expression of painrelated behavior in animals with peripheral neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective and antinociceptive effects of rosemary (Rosmarinus officinalis L.) extract in rats with painful diabetic neuropathy

et al. 2018

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Diabetes mellitus is associated with the development of neuronal tissue damage in different central and peripheral nervous system regions. A common complication of diabetes is painful diabetic peripheral neuropathy. We have explored the antihyperalgesic and neuroprotective properties of Rosmarinus officinalis L. extract (RE) in a rat model of streptozotocin (STZ)-induced diabetes. The nociceptive threshold and motor coordination of these diabetic rats was assessed using the tail-flick and rotarod treadmill tests, respectively. Activated caspase-3 and the Bax:Bcl-2 ratio, both biochemical indicators of apoptosis, were assessed in the dorsal half of the lumbar spinal cord tissue by western blotting. Treatment of the diabetic rats with RE improved hyperglycemia, hyperalgesia and motor deficit, suppressed caspase-3 activation and reduced the Bax:Bcl-2 ratio, suggesting that the RE has antihyperalgesic and neuroprotective effects in this rat model of STZ-induced diabetes. Cellular mechanisms underlying the observed effects may, at least partially, be related to the inhibition of neuronal apoptosis.

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“…In general, caspase-3 is the major executioner caspase in the caspase-dependent pathway ( 74 ) . Meanwhile, apoptotic pathways are mainly classified into the intrinsic (mitochondrial) pathway and the extrinsic (death ligand) pathway, and these classifications could be regulated by caspase-9 and caspase-8, respectively ( 75 ) . In this study, dietary glycinin exposure increased the mRNA levels of all of the apoptosis signalling, including caspase-3 , caspase-8 and caspase-9 in the DI of juvenile fish, whereas it decreased caspase-8 and caspase-9 mRNA levels in the PI and MI of fish.…”

Section: Discussionmentioning

confidence: 99%

Soyabean glycinin depresses intestinal growth and function in juvenile Jian carp (Cyprinus carpiovar Jian): protective effects of glutamine

Jiang

Zhang

et al. 2015

Br J Nutr

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This study investigated the effects of glycinin on the growth, intestinal oxidative status, tight junction components, cytokines and apoptosis signalling factors of fish. The results showed that an 80 g/kg diet of glycinin exposure for 42 d caused poor growth performance and depressed intestinal growth and function of juvenile Jian carp (Cyprinus carpio var. Jian). Meanwhile, dietary glycinin exposure induced increases in lipid peroxidation and protein oxidation; it caused reductions in superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) activities; and it increased MnSOD, CuZnSOD, GPx1b and GPx4a mRNA levels, suggesting an adaptive mechanism against stress in the intestines of fish. However, dietary glycinin exposure decreased both the activity and mRNA levels of nine isoforms of glutathione-S-transferase (GST) (α, μ, π, ρ, θ, κ, mGST1, mGST2 and mGST3), indicating toxicity to this enzyme activity and corresponding isoform gene expressions. In addition, glycinin exposure caused partial disruption of intestinal cell-cell tight junction components, disturbances of cytokines and induced apoptosis signalling in the distal intestines > mid intestines > proximal intestines of fish. Glycinin exposure also disturbed the mRNA levels of intestinalrelated signalling factors Nrf2, Keap1a, Keap1b, eleven isoforms of protein kinase C and target of rapamycin/4E-BP. Interestingly, glutamine was observed to partially block those negative influences. In conclusion, this study indicates that dietary glycinin exposure causes intestinal oxidative damage and disruption of intestinal physical barriers and functions and reduces fish growth, but glutamine can reverse those negative effects in fish. This study provides some information on the mechanism of glycinin-induced negative effects.

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Involvement of caspase-8, -9, and -3 in high glucose-induced apoptosis in PC12 cells

Cited by 8 publications

References 0 publications

Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels

Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels

Neuroprotective and antinociceptive effects of rosemary (Rosmarinus officinalis L.) extract in rats with painful diabetic neuropathy

Soyabean glycinin depresses intestinal growth and function in juvenile Jian carp (Cyprinus carpiovar Jian): protective effects of glutamine

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