PDF(Pubmed)
Abstract：
UNASSIGNED: In China, HUANGQI is widely used for the treatment of Alzheimer\'s disease (AD). However, a comprehensive understanding of its mechanism of anti-AD effects is lacking.
UNASSIGNED: To explore the active ingredients of HUANGQI and its potential targets and mechanisms of action in AD.
UNASSIGNED: The active ingredients and targets of HUANGQI were screened from databases (TCSMP, ETCM, and BATMan), and AD-related genes were obtained from DrugBank and GeneCards. The same target genes were screened, and a drug-target disease network was constructed. The PPI network was constructed and GO and KEGG pathway enrichment analyses of the targets. The Cell Counting Kit-8 (CCK-8) assay was used to determine suitable HUANGQI treatment concentrations for HT-22 cells between 0-480 μg/mL. CCK-8, FITC-phalloidin and propidium iodide (PI) assays were used to examine the protective effect of (0, 60, 120, 240 μg/mL) of HUANGQI on 20 μM Aβ1-42-induced HT-22 cell cytotoxicity.
UNASSIGNED: Twelve active ingredients of HUANGQI were selected, with 679 common targets associated with AD. GO and KEGG analysis revealed that the therapeutic mechanisms of HUANGQI involve TNF, AGE, the NF-κB pathway, and nuclear receptor activity-related processes. The CCK-8 assay indicated that HUANGQI was not cytotoxic to HT-22 cells at concentrations less than 240 μg/mL and was able to attenuate Aβ1-42-induced cellular damage (EC50 = 83.46 μg/mL). FITC-phalloidin and PI assays suggested that HUANGQI could alleviate 20 μM Aβ1-42-induced neuronal cell cytotoxicity in a dose-dependent manner.
UNASSIGNED: HUANGQI has a protective effect on Aβ1-42-induced nerve cell injury; further mechanism research was needed.
UNASSIGNED: To explore the active ingredients of HUANGQI and its potential targets and mechanisms of action in AD.
UNASSIGNED: The active ingredients and targets of HUANGQI were screened from databases (TCSMP, ETCM, and BATMan), and AD-related genes were obtained from DrugBank and GeneCards. The same target genes were screened, and a drug-target disease network was constructed. The PPI network was constructed and GO and KEGG pathway enrichment analyses of the targets. The Cell Counting Kit-8 (CCK-8) assay was used to determine suitable HUANGQI treatment concentrations for HT-22 cells between 0-480 μg/mL. CCK-8, FITC-phalloidin and propidium iodide (PI) assays were used to examine the protective effect of (0, 60, 120, 240 μg/mL) of HUANGQI on 20 μM Aβ1-42-induced HT-22 cell cytotoxicity.
UNASSIGNED: Twelve active ingredients of HUANGQI were selected, with 679 common targets associated with AD. GO and KEGG analysis revealed that the therapeutic mechanisms of HUANGQI involve TNF, AGE, the NF-κB pathway, and nuclear receptor activity-related processes. The CCK-8 assay indicated that HUANGQI was not cytotoxic to HT-22 cells at concentrations less than 240 μg/mL and was able to attenuate Aβ1-42-induced cellular damage (EC50 = 83.46 μg/mL). FITC-phalloidin and PI assays suggested that HUANGQI could alleviate 20 μM Aβ1-42-induced neuronal cell cytotoxicity in a dose-dependent manner.
UNASSIGNED: HUANGQI has a protective effect on Aβ1-42-induced nerve cell injury; further mechanism research was needed.
摘要：
■在中国，中药广泛应用于阿尔茨海默病(AD)的治疗。然而,缺乏对其抗AD作用机制的全面了解。
■探讨黄芪的有效成分及其在AD中的潜在作用靶点和作用机制。
■从数据库中筛选了黄芪的活性成分和靶标（TCSMP，ETCM,和BATMan),和AD相关基因从DrugBank和GeneCards获得。筛选相同的靶基因，构建了药物-目标疾病网络。构建PPI网络，并对靶标进行GO和KEGG途径富集分析。细胞计数试剂盒-8(CCK-8)测定用于确定0-480μg/mL之间的HT-22细胞的合适的黄芪处理浓度。CCK-8，FITC-phalalloidin和碘化丙啶（PI）测定法用于检测黄芩（0、60、120、240μg/mL）对20μMAβ1-42诱导的HT-22细胞的保护作用。细胞毒性。
■选择了12种黄芪活性成分，与AD相关的679个常见目标。GO和KEGG分析显示黄芩的治疗机制与TNF、年龄,NF-κB通路，和核受体活性相关的过程。CCK-8实验表明，在浓度低于240μg/mL时，黄芪对HT-22细胞没有细胞毒性，并且能够减轻Aβ1-42诱导的细胞损伤（EC50=83.46μg/mL）。FITC-phalloidin和PI测定表明，黄芩可以减轻20μMAβ1-42诱导的神经元细胞毒性，呈剂量依赖性。
■黄芩对Aβ1-42诱导的神经细胞损伤具有保护作用，需要进一步的机制研究。
■探讨黄芪的有效成分及其在AD中的潜在作用靶点和作用机制。
■从数据库中筛选了黄芪的活性成分和靶标（TCSMP，ETCM,和BATMan),和AD相关基因从DrugBank和GeneCards获得。筛选相同的靶基因，构建了药物-目标疾病网络。构建PPI网络，并对靶标进行GO和KEGG途径富集分析。细胞计数试剂盒-8(CCK-8)测定用于确定0-480μg/mL之间的HT-22细胞的合适的黄芪处理浓度。CCK-8，FITC-phalalloidin和碘化丙啶（PI）测定法用于检测黄芩（0、60、120、240μg/mL）对20μMAβ1-42诱导的HT-22细胞的保护作用。细胞毒性。
■选择了12种黄芪活性成分，与AD相关的679个常见目标。GO和KEGG分析显示黄芩的治疗机制与TNF、年龄,NF-κB通路，和核受体活性相关的过程。CCK-8实验表明，在浓度低于240μg/mL时，黄芪对HT-22细胞没有细胞毒性，并且能够减轻Aβ1-42诱导的细胞损伤（EC50=83.46μg/mL）。FITC-phalloidin和PI测定表明，黄芩可以减轻20μMAβ1-42诱导的神经元细胞毒性，呈剂量依赖性。
■黄芩对Aβ1-42诱导的神经细胞损伤具有保护作用，需要进一步的机制研究。
