Ginsenoside Rg1 and Acori Graminei Rhizoma Attenuates Neuron Cell Apoptosis by Promoting the Expression of miR-873-5p in Alzheimer’s Disease

• Published in: Neurochemical research Vol. 43; no. 8; pp. 1529 - 1538
• Main Authors: Shi, Ran, Zhang, Sishuo, Cheng, Guangqing, Yang, Xiaoni, Zhao, Ningning, Chen, Chao
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.08.2018; Springer Nature B.V
• Subjects: Alzheimer Disease - drug therapy; Alzheimer's disease; Animals; Apoptosis; Apoptosis - drug effects; Base Sequence; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cognitive ability; Drugs, Chinese Herbal - therapeutic use; Etiology; Gene expression; Gene Expression Regulation - drug effects; Ginsenosides; Ginsenosides - therapeutic use; Health risks; Heme Oxygenase-1 - genetics; Heme Oxygenase-1 - metabolism; Herbal medicine; Hippocampus - drug effects; Male; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; MicroRNAs - genetics; Neurochemistry; Neurology; Neurons - drug effects; Neuroprotective Agents - therapeutic use; Neurosciences; Nootropic Agents - therapeutic use; Original Paper; PC12 Cells; Pheochromocytoma cells; Rats; Ginsenoside Rg1; Acori graminei Rhizoma; Alzheimer’s disease; MiR-873-5p; Cell apoptosis
• ISSN: 0364-3190; 1573-6903; 1573-6903
• DOI: 10.1007/s11064-018-2567-y

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.