Astragaloside-IV regulates endoplasmic reticulum stress-mediated neuronal apoptosis in a murine model of Parkinson's disease via the lincRNA-p21/CHOP pathway
Abstract
Astragaloside-IV (AS-IV) protects the nerve cells of Parkinson's disease (PD) from damage. Long non-coding RNA (lincRNA) has been found to be important for many diseases. Lincnra-p21 is abnormally expressed in PD. The purpose of this study was to investigate whether Astragaloside-IV (AS-IV) affects endoplasmic reticulum stress (ERS)-induced neuronal apoptosis in PD, and its possible mechanisms. The PD mouse model was established via injecting 1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP) and the PD cell model was established via inducing the MN9D cell line with 1-methyl-4-pehnyl-pyridine (MPP+). The behavioral testing of PD model mice was tested after AS-IV treatment and PD-related lincRNAs expression were detected by qRT-PCR. After treatment of PD model cells with AS-IV, lincRNA-p21 expression was detected by qRT-PCR, and cell viability and apoptosis were detected by MTT assay and flow cytometry, respectively. The binding of lincRNA-p21 to C/EBP-homologous (CHOP) protein was investigated by RNA immunoprecipitation and RNA pull-down, and the effect of lincRNA-p21 on the ubiquitination of CHOP protein was examined by ubiquitination assay. The role of lincRNA-p21 in PD model was studied by cell transfection. In PD mice,...Continue Reading
References
Zonisamide suppresses endoplasmic reticulum stress-induced neuronal cell damage in vitro and in vivo
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Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis