Cornus officinalis Extracts Alleviate Amyloid Beta-Peptide 25-35-Induced Nerve Cell Injury in Alzheimer’s Disease by Upregulating Long Non-Coding RNA Rpph1

Abstract

To explore the protective effect of Cornus officinalis extracts on Alzheimer’s disease cell injury models and its underlying molecular mechanism. Pheochromocytoma cells were treated with 20 μM amyloid beta-peptide 25-35 to establish an Alzheimer’s disease cell injury model in vitro, which was recorded as amyloid beta-peptide 25-35 group. Cells affected by amyloid beta-peptide 25-35 were treated with different-doses of Cornus officinalis extracts and recorded as low-dose Cornus officinalis extracts group, medium-dose Cornus officinalis extracts group and high-dose Cornus officinalis extracts group. Pheochromocytoma cells transfected with si-NC/si-long non-coding RNA Rpph1, treated with 20 μM amyloid beta-peptide 25-35 and 80 mg/ml of Cornus officinalis extracts were recorded as high-dose Cornus officinalis extracts+si-NC group, high-dose Cornus officinalis extracts+si-long non-coding RNA Rpph1 group. Cell viability and apoptosis were examined using cell counting kit-8 assay and flow cytometry. Protein expression was tested by Western blot. Malondialdehyde, superoxide dismutase and catalase levels were assessed by measuring cell oxidative stress. Amyloid beta-peptide, tumor necrosis factor-alpha, interleukin-6 and interferon gamma levels were examined using enzyme-linked immunosorbent assay. Long non-coding RNA Rpph1 expression was detected using quantitative reverse transcriptase polymerase chain reaction. Amyloid beta-peptide 25-35 treatment decreased Pheochromocytoma cell viability, CyclinD1, superoxide dismutase, catalase and long non-coding RNA Rpph1 levels, while increased apoptosis rate, cleaved-caspase-3, malondialdehyde, amyloid beta-peptide, tumor necrosis factor-alpha, interleukin-6 and interferon gamma levels. After treatment with different-doses of Cornus officinalis extracts, cell viability, CyclinD1, superoxide dismutase, catalase and long non-coding RNA Rpph1 levels were enhanced, while apoptosis rate, cleaved-caspase-3, malondialdehyde, Aβ, tumor necrosis factor-alpha, interleukin-6 and interferon gamma levels were reduced in pheochromocytoma cells treated with amyloid beta-peptide 25-35. Downregulation of long non-coding RNA Rpph1 reversed the inhibitory effect of Cornus officinalis extracts on cell injury. Cornus officinalis extracts relieved amyloid beta-peptide 25-35-induced nerve cell injury by upregulating long non-coding RNA Rpph1, suggesting that Cornus officinalis extracts might be used in Alzheimer's disease treatment.