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首页> 外文期刊>Neurochemical research >Ginsenoside Rg1 and Acori Graminei Rhizoma Attenuates Neuron Cell Apoptosis by Promoting the Expression of miR-873-5p in Alzheimer’s Disease
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Ginsenoside Rg1 and Acori Graminei Rhizoma Attenuates Neuron Cell Apoptosis by Promoting the Expression of miR-873-5p in Alzheimer’s Disease

机译:人参皂甙RG1和Acori Graminei Rhizoma通过促进Alzheimer疾病的miR-873-5p的表达来衰减神经元细胞凋亡

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摘要

Alzheimer’s disease (AD) severely threatens human health in their old age, however the potential etiology underlying it is still unclear. Both Ginsenoside Rg1 (GRg1) and Acori graminei Rhizoma (AGR) are the traditional Chinese herbal drug, while their potential role in AD remains need further identification. Both SAMP1 and SAMP8 mice were employed as the control and AD mice. Morris water maze method was used to detect the cognitive function of the mice, TUNEL assay was performed to determine cell apoptosis. Real-time PCR and western blot were carried out to measure gene expression. The relationship between miR-873-5p and HMOX1 was determined using luciferase reporter assay. Comparing with SAMP1, the cognitive function was impaired and cell apoptosis was increased in SAMP8 mice. GRg1?+?AGR treatment significantly attenuated the symptom of AD. The expression of miR-873-5p was decreased, while HMOX1 was increased in SAMP8 mice. GRg1?+?AGR treatment significantly promoted the expression of miR-873-5p, but decreased HMOX1. MiR-873-5p targets HMOX1 to regulate its expression. Aβ1–42 stimulation decreased the expression of miR-873-5p, but increased HMOX1 in PC12 cells. GRg1?+?AGR treatment reversed the effect of Aβ1–42, while miR-873-5p inhibitor abolished the effect of GRg1?+?AGR. In vivo experiments confirmed the protect role of GRg1?+?AGR in AD. GRg1?+?AGR suppressed neuron cell apoptosis by regulating the expression of miR-873-5p in AD.
机译:阿尔茨海默病的疾病(AD)严重威胁到年龄的人类健康,然而它仍然不清楚的潜在病因。人参皂苷RG1(GRG1)和Acori Graminei Rhizoma(AGRI)是中草药,而他们在AD中的潜在作用仍然需要进一步鉴定。 SAMP1和SAMP8小鼠均用作对照和AD小鼠。 Morris水迷宫法用于检测小鼠的认知功能,进行TUNEL测定以确定细胞凋亡。进行实时PCR和Western印迹以测量基因表达。使用荧光素酶报告器测定法测定miR-873-5p和hMox1之间的关系。与SAMP1相比,认知功能受损,SAMP8小鼠中的细胞凋亡增加。 grg1?+ x + act治疗明显减弱了广告的症状。 MiR-873-5P的表达降低,而HMOX1在SAMP8小鼠中增加。 GRG1?+ +植物治疗明显促进了miR-873-5p的表达,但下降了HMOX1。 mir-873-5p靶向hmox1以调节其表达。 Aβ1-42刺激降低了MiR-873-5P的表达,但在PC12细胞中增加了HMOX1。 GRG1?+ + _耕作治疗逆转Aβ1-42的效果,而MIR-873-5P抑制剂废除GRG1的效果?+ + _ {agr。体内实验证实了GRG1的保护作用?+在广告中agr。 GRG1?+ +抑制ADS中miR-873-5p的表达抑制神经元细胞凋亡。

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