Dataset Information

Neuroprotective Effects and Mechanism of ?-Asarone against A?1-42-Induced Injury in Astrocytes.

ABSTRACT: Emerging evidence suggests that activated astrocytes play important roles in AD, and ?-asarone, a major component of Acorus tatarinowii Schott, was shown to be a potential therapeutic candidate for AD. While our previous study found that ?-asarone could improve the cognitive function of rats hippocampally injected with A?, the effects of ?-asarone on astrocytes remain unclear, and this study aimed to investigate these effects. A rat model of A?1-42 (10??g) was established, and the rats were intragastrically treated with ?-asarone at doses of 10, 20, and 30?mg/kg or donepezil at a dose of 0.75?mg/kg. The sham and model groups were intragastrically injected with an equal volume of saline. Animals were sacrificed on the 28th day after administration of the drugs. In addition, a cellular model of A?1-42 (1.1??M, 6?h) was established, and cells were treated with ?-asarone at doses of 0, 2.06, 6.17, 18.5, 55.6, and 166.7??g/mL. ?-Asarone improved cognitive impairment, alleviated A? deposition and hippocampal damage, and inhibited GFAP, AQP4, IL-1?, and TNF-? expression. These results suggested that ?-asarone could alleviate the symptoms of AD by protecting astrocytes, possibly by inhibiting TNF-? and IL-1? secretion and then downregulating AQP4 expression.

SUBMITTER: Yang Y

PROVIDER: S-EPMC5828282 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Publications

Neuroprotective Effects and Mechanism of β-Asarone against Aβ1-42-Induced Injury in Astrocytes.

Yang Yuanxiao Y Xuan Ling L Chen Hongshu H Dai Shijie S Ji Liting L Bao Yuting Y Li Changyu C

Evidence-based complementary and alternative medicine : eCAM 20171128

Emerging evidence suggests that activated astrocytes play important roles in AD, and β-asarone, a major component of Acorus tatarinowii Schott, was shown to be a potential therapeutic candidate for AD. While our previous study found that β-asarone could improve the cognitive function of rats hippocampally injected with Aβ, the effects of β-asarone on astrocytes remain unclear, and this study aimed to investigate these effects. A rat model of Aβ1-42 (10 < ...[more]

PMID: 29599803

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Project description:BACKGROUND:Spinal cord injury (SCI) is a destructive disease that incurs huge personal and social costs, and there is no effective treatment. Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus, the pathogenesis of SCI is still under investigation. AIM:To determine the key genes based on the modularization of in-depth analysis, in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI. METHODS:Firstly, the differences between injured and non-injured spinal cord of astrocyte (HA), injured and non-injured spinal cord of non-astrocyte (FLOW), injured spinal cord of non-injured astrocyte (HA) and non-injured spinal cord of non-astrocyte (FLOW), and non-injured spinal cord of astrocyte (HA) and non-astrocyte (FLOW) were analyzed. The total number of differentially expressed genes was obtained by merging the four groups of differential results. Secondly, the genes were co-expressed and clustered. Then, the enrichment of GO function and KEGG pathway of module genes was analyzed. Finally, non-coding RNA, transcription factors and drugs that regulate module genes were predicted using hypergeometric tests. RESULTS:In summary, we obtained 19 expression modules involving 5216 differentially expressed genes. Among them, miR-494, XIST and other genes were differentially expressed in SCI patients, and played an active regulatory role in dysfunction module, and these genes were recognized as the driving genes of SCI. Enrichment results showed that module genes were significantly involved in the biological processes of inflammation, oxidation and apoptosis. Signal pathways such as NF-kappa B/A20, AMPK and MAPK were significantly regulated. In addition, non-coding RNA pivot (including miR-136-5p and let-7d-5p, etc.) and transcription factor pivot (including NFKB1, MYC, etc.) were identified as significant regulatory dysfunction modules. CONCLUSION:Overall, this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI. These findings helped to reveal the core dysfunction modules, potential regulatory factors and driving genes of the disease, and to improve our understanding of its pathogenesis.

Dataset Information

Neuroprotective Effects and Mechanism of ?-Asarone against A?1-42-Induced Injury in Astrocytes.

Publications

Neuroprotective Effects and Mechanism of <i>β</i>-Asarone against A<i>β</i>1-42-Induced Injury in Astrocytes.

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