Pan, Yj., Gu, Yj. & Gu, Xs. Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell., CJIM 8, 200–203 (2002). https://doi.org/10.1007/BF02934310
Yong-jin Pan, Yong-jian Gu, Xiao-su Gu. Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell. [J]. Chinese Journal of Integrative Medicine 8(3):200-203(2002)
Pan, Yj., Gu, Yj. & Gu, Xs. Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell., CJIM 8, 200–203 (2002). https://doi.org/10.1007/BF02934310DOI:
Yong-jin Pan, Yong-jian Gu, Xiao-su Gu. Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell. [J]. Chinese Journal of Integrative Medicine 8(3):200-203(2002) DOI: 10.1007/BF02934310.
Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell
摘要
To study the effect of Acanthopanax senticosus saponin (ASS) on free radical injury induced neuron aging. On day 7 of fetal mice
cortical neuron primary passage cultures were divided into the normal control group
model group and ASS groups. The model group using free radical (FeSO4 plus H2O2) injury mode prepared in vivo cultured ICR mice cortical neuron aging model; ASS groups: 24 hrs before and after treated with H2O2 and FeSO4
different concentration of ASS was added
according to biochemical parameters such as lactate dehydrogenase (LDH)
superoxide dismutase (SOD) and malondialdehyde (MDA) etc. and histomorphologic change to observe the protection of ASS on aging neurons. The LDH
SOD
MDA of the model group were compared with the normal group
< 0. 01; ASS groups added 1.25 mg/100 ml
2.5 mg/100 ml
5 mg/100 ml concentration of ASS
their LDH
SOD
MDA compared with the model group π.05-0.01
the difference was significant. In medicated groups the SOD activity of oxidization injured nerve cells obviously elevated
LDH activity and MDA content apparently lowered. Microscope and scanning electron microscopic observation showed that supplemented with ASS to protect the nerve cell injury abated
part of the cellular structure tended to normalize. ASS could act against free radical toxic effect
increase the anti-oxidase activity
strengthen the protection of neuron cells. It is assumed that the effect against nerve cell aging was possibly through scavenging oxygen free radical
strengthening the stability of cell membrane
thus delaying the development of aging.
Abstract
To study the effect of Acanthopanax senticosus saponin (ASS) on free radical injury induced neuron aging. On day 7 of fetal mice
cortical neuron primary passage cultures were divided into the normal control group
model group and ASS groups. The model group using free radical (FeSO4 plus H2O2) injury mode prepared in vivo cultured ICR mice cortical neuron aging model; ASS groups: 24 hrs before and after treated with H2O2 and FeSO4
different concentration of ASS was added
according to biochemical parameters such as lactate dehydrogenase (LDH)
superoxide dismutase (SOD) and malondialdehyde (MDA) etc. and histomorphologic change to observe the protection of ASS on aging neurons. The LDH
SOD
MDA of the model group were compared with the normal group
< 0. 01; ASS groups added 1.25 mg/100 ml
2.5 mg/100 ml
5 mg/100 ml concentration of ASS
their LDH
SOD
MDA compared with the model group π.05-0.01
the difference was significant. In medicated groups the SOD activity of oxidization injured nerve cells obviously elevated
LDH activity and MDA content apparently lowered. Microscope and scanning electron microscopic observation showed that supplemented with ASS to protect the nerve cell injury abated
part of the cellular structure tended to normalize. ASS could act against free radical toxic effect
increase the anti-oxidase activity
strengthen the protection of neuron cells. It is assumed that the effect against nerve cell aging was possibly through scavenging oxygen free radical
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