FOLLOWUS
1. Department of Traditional Chinese Medicine, Translational Medicine Center, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences,Beijing,China
2. Department of Pathology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College,Beijing,China
纸质出版日期:2017,
网络出版日期:2017-9-2,
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Shi, Y., Liang, Xc., Zhang, H. et al. Combination of quercetin, cinnamaldehyde and hirudin protects rat dorsal root ganglion neurons against high glucose-induced injury through Nrf-2/HO-1 activation and NF-κB inhibition., Chin. J. Integr. Med. 23, 663–671 (2017). https://doi.org/10.1007/s11655-017-2405-0
Yue Shi, Xiao-chun Liang, Hong Zhang, et al. Combination of quercetin, cinnamaldehyde and hirudin protects rat dorsal root ganglion neurons against high glucose-induced injury through Nrf-2/HO-1 activation and NF-κB inhibition[J]. Chinese Journal of Integrative Medicine, 2017,23(9):663-671.
Shi, Y., Liang, Xc., Zhang, H. et al. Combination of quercetin, cinnamaldehyde and hirudin protects rat dorsal root ganglion neurons against high glucose-induced injury through Nrf-2/HO-1 activation and NF-κB inhibition., Chin. J. Integr. Med. 23, 663–671 (2017). https://doi.org/10.1007/s11655-017-2405-0 DOI:
Yue Shi, Xiao-chun Liang, Hong Zhang, et al. Combination of quercetin, cinnamaldehyde and hirudin protects rat dorsal root ganglion neurons against high glucose-induced injury through Nrf-2/HO-1 activation and NF-κB inhibition[J]. Chinese Journal of Integrative Medicine, 2017,23(9):663-671. DOI: 10.1007/s11655-017-2405-0.
To examine the effects of the combination of quercetin (Q)
cinnamaldehyde (C) and hirudin (H)
a Chinese medicine formula on high glucose (HG)-induced apoptosis of cultured dorsal root ganglion (DRG) neurons. DRG neurons exposed to HG (45 mmol/L) for 24 h were employed as an in vitro model of diabetic neuropathy. Cell viability
reactive oxygen species (ROS) level and apoptosis were determined. The expression of nuclear factor of Kappa B (NF-κB)
inhibitory kappa Bα(IκBα)
phosphorylated IκBα and Nf-E2 related factor 2 (Nrf2) were examined using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot assay. The expression of hemeoxygenase-1 (HO-1)
interleukin-6 (IL-6)
tumor necrosis factor (TNF-α) and caspase-3 were also examined by RT-PCR and Western blot assay. HG treatment markedly increased DRG neuron apoptosis via increasing intracellular ROS level and activating the NF-κB signaling pathway (P<0.05). Co-treatment with Q
C
H and their combination decreased HG-induced caspase-3 activation and apoptosis (P<0.05 or P<0.01). The expressions of NF-κB
IL-6 and TNF-α were down-regulated
and Nrf2/HO-1 expression was up-regulated (P<0.05 or P<0.01). QCH has better effect in scavenging ROS
activating Nrf-2/HO-1
and down-regulating the NF-κB pathway than other treatment group. DRG neurons' apoptosis was increased in diabetic conditions
which was reduced by QCH formula treatment. The possible reason could be activating Nrf-2/HO-1 pathway
scavenging ROS
and inhibition of NF-κB activation. The effect of QCH combination was better than each monomer or the combination of the two monomers.
To examine the effects of the combination of quercetin (Q)
cinnamaldehyde (C) and hirudin (H)
a Chinese medicine formula on high glucose (HG)-induced apoptosis of cultured dorsal root ganglion (DRG) neurons. DRG neurons exposed to HG (45 mmol/L) for 24 h were employed as an in vitro model of diabetic neuropathy. Cell viability
reactive oxygen species (ROS) level and apoptosis were determined. The expression of nuclear factor of Kappa B (NF-κB)
inhibitory kappa Bα(IκBα)
phosphorylated IκBα and Nf-E2 related factor 2 (Nrf2) were examined using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot assay. The expression of hemeoxygenase-1 (HO-1)
interleukin-6 (IL-6)
tumor necrosis factor (TNF-α) and caspase-3 were also examined by RT-PCR and Western blot assay. HG treatment markedly increased DRG neuron apoptosis via increasing intracellular ROS level and activating the NF-κB signaling pathway (P<0.05). Co-treatment with Q
C
H and their combination decreased HG-induced caspase-3 activation and apoptosis (P<0.05 or P<0.01). The expressions of NF-κB
IL-6 and TNF-α were down-regulated
and Nrf2/HO-1 expression was up-regulated (P<0.05 or P<0.01). QCH has better effect in scavenging ROS
activating Nrf-2/HO-1
and down-regulating the NF-κB pathway than other treatment group. DRG neurons' apoptosis was increased in diabetic conditions
which was reduced by QCH formula treatment. The possible reason could be activating Nrf-2/HO-1 pathway
scavenging ROS
and inhibition of NF-κB activation. The effect of QCH combination was better than each monomer or the combination of the two monomers.
diabetic peripheral neuropathyoxidative stressapoptosisdorsal root ganglion neuronsChinese Herb
diabetic peripheral neuropathyoxidative stressapoptosisdorsal root ganglion neuronsChinese Herb
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