Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling

Kulebyakin, Konstantin; Karpova, L.V.; Lakonsteva, Ekaterina; Krasavin, Mikhail; Boldyrev, Alexander A.

doi:10.1007/s00726-011-1135-4

Cited by 35 publications

(28 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The prolonged activation of ERK 1/2 in PC12 cells by H 2 O 2 revealed by us is in agreement with data showing the activation of this enzyme by reactive oxygen species [27–29]. Pre-incubation with nanomolar and micromolar α-T for 18 h did not change the initial activation of ERK 1/2 during the first 20 min after PC12 cell exposure to H 2 O 2 , but it markedly decreased the time of maximal activation of ERK 1/2 by H 2 O 2 .…”

Section: Resultssupporting

confidence: 92%

“…Pre-incubation with nanomolar and micromolar α-T for 18 h did not change the initial activation of ERK 1/2 during the first 20 min after PC12 cell exposure to H 2 O 2 , but it markedly decreased the time of maximal activation of ERK 1/2 by H 2 O 2 . It is of interest that the similar effect of carnosine on ERK 1/2 activity was recently described, carnosine was shown to protect cerebellar granule cells against oxidative stress and to decrease the time of ERK 1/2 activation [29]. Such an effect of α-T in our studies may result from activation of protein phosphatases, especially 2A [3,4,30].…”

Section: Resultssupporting

confidence: 66%

“…However, the simple explanation that ERK activation increases the cell survival of cortical neurons, while its inhibition leads to their death, does not work in this model [17], as in our case. As hydrogen peroxide is known to activate ERK 1/2 [27–29] the inhibition of ERK 1/2 activity by MEK 1/2 inhibitor (UO126) could be suggested (according to such an explanation) to result in a marked decrease of the viability of the cortical neurons. However, the experimental data obtained by Numakawa and co-authors show that MEK 1/2 inhibitor does not diminish the viability of cortical neurons exposed to H 2 O 2 .…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Захарова

Sokolova²,

Bayunova³

et al. 2012

IJMS

View full text Add to dashboard Cite

The aim of this work was to compare protective and anti-apoptotic effects of α-tocopherol at nanomolar and micromolar concentrations against 0.2 mM H2O2-induced toxicity in the PC12 neuronal cell line and to reveal protein kinases that contribute to α-tocopherol protective action. The protection by 100 nM α-tocopherol against H2O2-induced PC12 cell death was pronounced if the time of pre-incubation with α-tocopherol was 3–18 h. For the first time, the protective effect of α-tocopherol was shown to depend on its concentration in the nanomolar range (1 nM < 10 nM < 100 nM), if the pre-incubation time was 18 h. Nanomolar and micromolar α-tocopherol decreased the number of PC12 cells in late apoptosis induced by H2O2 to the same extent if pre-incubation time was 18 h. Immunoblotting data showed that α-tocopherol markedly diminished the time of maximal activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and protein kinase B (Akt)-induced in PC12 cells by H2O2. Inhibitors of MEK 1/2, PI 3-kinase and protein kinase C (PKC) diminished the protective effect of α-tocopherol against H2O2-initiated toxicity if the pre-incubation time was long. The modulation of ERK 1/2, Akt and PKC activities appears to participate in the protection by α-tocopherol against H2O2-induced death of PC12 cells. The data obtained suggest that inhibition by α-tocopherol in late stage ERK 1/2 and Akt activation induced by H2O2 in PC12 cells makes contribution to its protective effect, while total inhibition of these enzymes is not protective.

show abstract

Section: Resultssupporting

confidence: 92%

Section: Resultssupporting

confidence: 66%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Захарова

Sokolova²,

Bayunova³

et al. 2012

IJMS

View full text Add to dashboard Cite

show abstract

“…Histidine has beneficial effects on liver and lung injury in rats and has been reported to protect against diabetic complications in a mouse model of diabetes through its actions against oxidative stress [25][26][27]. It can restrict accumulation of free radicals and delay activation of extracellular signalregulated kinase and c-jun N terminal kinase in neuronal cells [28].…”

Section: Discussionmentioning

confidence: 99%

Histidine supplementation improves insulin resistance through suppressed inflammation in obese women with the metabolic syndrome: a randomised controlled trial

et al. 2013

View full text Add to dashboard Cite

Aims/hypothesis Increased inflammation and oxidative stress are associated with insulin resistance (IR) and metabolic disorders. Serum histidine levels are lower and are negatively associated with inflammation and oxidative stress in obese women. The objective of this study was to evaluate the efficacy of histidine supplementation on IR, inflammation, oxidative stress and metabolic disorders in obese women with the metabolic syndrome (MetS). Methods A total of 100 obese women aged 33-51 years with BMI≥28 kg/m 2 and diagnosed with MetS were included following a health examination in the community hospital in this randomised, double-blinded, placebo-controlled trial. Participants were allocated to interventions by an investigator using sequentially numbered sealed envelopes and received 4 g/day histidine (n=50) or identical placebo (n=50) for 12 weeks. Participants then attended the same clinic every 2 weeks for scheduled interviews and to count tablets returned. Serum histidine, HOMA-IR, BMI, waist circumference, fat mass, serum NEFA, and variables connected to inflammation and oxidative stress were measured at baseline and 12 weeks. Participants, examining physicians and investigators assessing the outcomes were blinded to group assignment. In addition, the inflammatory mechanisms of histidine were also explored in adipocytes. CI 0.60, 3.44] in histidine supplementation group (n=45), respectively. There were significant correlations between changes in serum histidine and changes of IR and its risk factors. No side effects were observed during the intervention. In vitro study indicated that histidine suppresses IL6 and TNF mRNA expression and nuclear factor kappa-B (NF-κB) protein production in palmitic acid-induced adipocytes in a dose-dependent manner, and these changes were diminished by an inhibitor of NF-κB. Conclusions/interpretation Histidine supplementation could improve IR, reduce BMI, fat mass and NEFA and suppress inflammation and oxidative stress in obese women with MetS; histidine could improve IR through suppressed pro-inflammatory cytokine expression, possibly by the NF-κB pathway, in adipocytes. Trial registration www.chictr.org/cn/ChiCTR-TRC-11001551Electronic supplementary material The online version of this article

show abstract

“…As expected, the levels of phosphorylation obtained when microglial cells were infected with ST7 strains were stronger than those obtained with ST1 strains. In addition to the MAPK contribution to cytokine release, this pathway also regulates oxidative stress, which can in turn induce cellular injury (Kulebyakin et al, 2012;Park et al, 2012). Oxidative stress can cause overexpression of antioxidant responsive factors in cells.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the pathogenesis of meningitis caused by Streptococcus suis sequence type 7 using the infection of BV2 microglial cells

Zheng

Sun

Domínguez-Punaro

et al. 2013

Journal of Medical Microbiology

View full text Add to dashboard Cite

Streptococcus suis is an important agent of swine and human meningitis. Among several sequence types (STs) characterized within the S. suis strain population, ST7 has emerged only in China and has been reported to be the cause of the human outbreak caused by S. suis in 2005. S. suis ST7 was shown to be derived from S. suis ST1 through a single-nucleotide change in the housekeeping gene thyA. The virulence potential of S. suis ST7 is reported to be higher than that of the worldwide-studied pathogenic S. suis ST1. The pathogenesis of ST1 infection has been partially elucidated, but information on the pathogenesis of ST7 infections remains scarce. To improve our understanding of the mechanisms involved in the development of meningitis caused by ST7, this study compared the microglial inflammatory response induced by ST1 and ST7 strains. The data showed that S. suis ST7 possessed a higher ability to induce pro-inflammatory cytokine production and to activate mitogen-activated protein kinase pathways and several transcription factors. The stimulation of microglial cells by S. suis increased the expression levels of the nucleotide oligomerization domain 2 (Nod2) gene. Finally, the results indicated that signal transducer and activator of transcription 3 (STAT-3) was involved in the development of meningitis induced by S. suis ST7 infection.

show abstract

Carnosine protects neurons against oxidative stress and modulates the time profile of MAPK cascade signaling

Cited by 35 publications

References 22 publications

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

α-Tocopherol at Nanomolar Concentration Protects PC12 Cells from Hydrogen Peroxide-Induced Death and Modulates Protein Kinase Activities

Histidine supplementation improves insulin resistance through suppressed inflammation in obese women with the metabolic syndrome: a randomised controlled trial

Evaluation of the pathogenesis of meningitis caused by Streptococcus suis sequence type 7 using the infection of BV2 microglial cells

Contact Info

Product

Resources

About