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 norm...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 (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. Results 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. 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.展开更多
Objective： To investigate the neuro-protective effects of Acanthopanax senticosus Harms（EAS） on mesencephalic mitochondria and the mechanism of action, using a mouse model of Parkinson＇s disease（PD）. Methods： T...Objective： To investigate the neuro-protective effects of Acanthopanax senticosus Harms（EAS） on mesencephalic mitochondria and the mechanism of action, using a mouse model of Parkinson＇s disease（PD）. Methods： The chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms（EAS） was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group, the MPTP model group, and the EAS treated group with MPTP（MPTP＋EAS group, 10 in each group）. The MPTP model group and the MPTP＋EAS group received MPTP-HCl（30 mg/kg i.p） once a day for 5 days. The control group received an equal volume of saline（20 m L/kg i.p） once a day for 5 days. Induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride daily（MPTP-HCl, 30 mg/kg） for 5 days, the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model, including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2（NDUFV2）, mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1（MT-ND1）, succinate dehydrogenase complex subunit A（SDHA）, and succinate dehydrogenase cytochrome b560 subunit（SDHC）. Results： After treatment with EAS, the behavioral changes induced by MPTP were attenuated significantly（P〈0.05）. EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential（both P〈0.05）, which was supported by an ultra-structural level analysis. The changes in reactive oxygen species（ROS）, malonic dialdehyde（MDA）, oxidative phosphorylation（OXPHOS） system 4 subunits levels and PD-related proteins expressions（parkin, Pink1, DJ-1, α-synuclein, and Lrrk2） reverted to near normal levels（all P〈0.05）, based on the results展开更多
AIM To examine the effects of Acanthopanax senticosus polysaccharides(ASPS) on intestinal tight junction(TJ) disruption and nuclear factor-kappa B(NF-κB)/myosin light chain kinase(MLCK) activation in endotoxemia.METH...AIM To examine the effects of Acanthopanax senticosus polysaccharides(ASPS) on intestinal tight junction(TJ) disruption and nuclear factor-kappa B(NF-κB)/myosin light chain kinase(MLCK) activation in endotoxemia.METHODS BALB/C mice(6-8-weeks-old) received continuous intragastric gavage of ASPS for 7 d before injection of lipopolysaccharide(LPS), or received ASPS once after LPS injection. Blood and intestinal mucosal samples were collected 6 h after LPS challenge. Clinical symptoms, histological injury, intestinal permeability,TJ ultrastructure, and TJ protein expression were determined.RESULTS Compared with mice in the LPS group, pretreatment with ASPS improved clinical and histological scores by 390.9%(P < 0.05) and 57.89%(P < 0.05), respectively, and gut permeability change in endotoxemic mice was shown by a 61.93% reduction in reduced leakage of fluorescein isothiocyanate-dextran 6 h after LPS injection(P < 0.05). ASPS pretreatment also prevented LPS-induced TJ ultrastructure breakdown supported by increased electron dense materials between adjoining cells, sustained redistribution and expression of occludin(0.597 ± 0.027 vs 0.103 ± 0.009, P < 0.05) and zonula occludens-1(0.507 ± 0.032 vs 0.125 ± 0.019, P < 0.05), and suppressed activation of the NF-κB/MLCK pathway indicated by reduced expression of NF-κB, phospho-inhibitor kappa B-alpha, MLCK and phospho-myosin light-chain-2 by 16.06%(P < 0.05), 54.31%(P < 0.05), 66.10%(P < 0.05) and 64.82%(P < 0.05), respectively. CONCLUSION ASPS pretreatment may be associated with inhibition of the NF-κB/MLCK pathway and concomitant amelioration of LPS-induced TJ dysfunction of intestinal epithelium in endotoxemia.展开更多
文摘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 (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. Results 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. 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.
基金Supported by the National Natural Science Foundation of China(No.81270056)China Postdoctoral Science Foundation(No.2013T60398)+2 种基金Scientific Research grants of Postdoctoral Researchers Settled in Heilongjiang(No.LBH-Q13160)Outstanding Talents Cultivation Fund of Heilongjiang University of Chinese Medicine(No.2013jc01)the Outstanding Innovative Talent Support Programs of Heilongjiang University of Chinese Medicine
文摘Objective： To investigate the neuro-protective effects of Acanthopanax senticosus Harms（EAS） on mesencephalic mitochondria and the mechanism of action, using a mouse model of Parkinson＇s disease（PD）. Methods： The chemical fingerprint analysis of the extract of Acanthopanax senticosus Harms（EAS） was performed using the ultra performance liquid chromatograph and time of flight mass spectrometry. Thirty mice were randomly divided into the control group, the MPTP model group, and the EAS treated group with MPTP（MPTP＋EAS group, 10 in each group）. The MPTP model group and the MPTP＋EAS group received MPTP-HCl（30 mg/kg i.p） once a day for 5 days. The control group received an equal volume of saline（20 m L/kg i.p） once a day for 5 days. Induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine hydrochloride daily（MPTP-HCl, 30 mg/kg） for 5 days, the PD mice were treated with EAS at 45.5 mg/kg daily for 20 days. The behavioral testing of mice was carried out using the pole-climbing test. The integrity and functions of neurons were examined in mesencephalic mitochondria in a PD mouse model, including nicotinamide adenine dinucleotide dehydrogenase ubiquinone flavoprotein 2（NDUFV2）, mitochondrially encoded nicotinamide adenine dinucleotide dehydrogenase 1（MT-ND1）, succinate dehydrogenase complex subunit A（SDHA）, and succinate dehydrogenase cytochrome b560 subunit（SDHC）. Results： After treatment with EAS, the behavioral changes induced by MPTP were attenuated significantly（P〈0.05）. EAS protected the mesencephalic mitochondria from swelling and attenuated the decreases in their membrane potential（both P〈0.05）, which was supported by an ultra-structural level analysis. The changes in reactive oxygen species（ROS）, malonic dialdehyde（MDA）, oxidative phosphorylation（OXPHOS） system 4 subunits levels and PD-related proteins expressions（parkin, Pink1, DJ-1, α-synuclein, and Lrrk2） reverted to near normal levels（all P〈0.05）, based on the results
文摘AIM To examine the effects of Acanthopanax senticosus polysaccharides(ASPS) on intestinal tight junction(TJ) disruption and nuclear factor-kappa B(NF-κB)/myosin light chain kinase(MLCK) activation in endotoxemia.METHODS BALB/C mice(6-8-weeks-old) received continuous intragastric gavage of ASPS for 7 d before injection of lipopolysaccharide(LPS), or received ASPS once after LPS injection. Blood and intestinal mucosal samples were collected 6 h after LPS challenge. Clinical symptoms, histological injury, intestinal permeability,TJ ultrastructure, and TJ protein expression were determined.RESULTS Compared with mice in the LPS group, pretreatment with ASPS improved clinical and histological scores by 390.9%(P < 0.05) and 57.89%(P < 0.05), respectively, and gut permeability change in endotoxemic mice was shown by a 61.93% reduction in reduced leakage of fluorescein isothiocyanate-dextran 6 h after LPS injection(P < 0.05). ASPS pretreatment also prevented LPS-induced TJ ultrastructure breakdown supported by increased electron dense materials between adjoining cells, sustained redistribution and expression of occludin(0.597 ± 0.027 vs 0.103 ± 0.009, P < 0.05) and zonula occludens-1(0.507 ± 0.032 vs 0.125 ± 0.019, P < 0.05), and suppressed activation of the NF-κB/MLCK pathway indicated by reduced expression of NF-κB, phospho-inhibitor kappa B-alpha, MLCK and phospho-myosin light-chain-2 by 16.06%(P < 0.05), 54.31%(P < 0.05), 66.10%(P < 0.05) and 64.82%(P < 0.05), respectively. CONCLUSION ASPS pretreatment may be associated with inhibition of the NF-κB/MLCK pathway and concomitant amelioration of LPS-induced TJ dysfunction of intestinal epithelium in endotoxemia.
