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Objective: To study the effect of Acanthopanax senticosus saponin (ASS) on free radical injury induced neuron aging. Methods: 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 (FeSO 4 plus H 2O 2) injury mode prepared in vivo cultured ICR mice cortical neuron aging model; ASS groups: 24 hrs before and after treated with H 2O 2 and FeSO 4, 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. Results: The LDH, SOD, MDA of the model group were compared with the normal group, P<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 P<0.05-0.01, 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. Conclusion: 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.
Objective: To study the effect of Acanthopanax senticosus saponin (ASS) on free radical injury induced neuron aging. Methods: 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 (FeSO 4 plus H 2O 2) injury mode prepared in vivo cultured ICR mice cortical neuron aging model; ASS groups: 24 hrs before and after treated with H 2O 2 and FeSO 4, different concentration of ASS was added, Based on 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. Results: The LDH, SOD, MDA of the model group were Compared with the normal group, P<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 P<0.05-0.01 , the difference was significant. In medicate d groups the SOD activity of oxidization sustained nerve cells increase 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, enhance 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, Delaying the development of aging.