ABSTRACT
OBJECTIVE: To investigate the specific role of long non-coding RNA (lncRNA) SETD5-AS1 in regulating stroke development, and its underlying mechanism. MATERIALS AND METHODS: Middle cerebral artery occlusion (MCAO) model and OGD/R (oxygen-glucose deprivation/reoxygenation) model were constructed for exploring the mechanism of ischemia-reperfusion injury induced by ischemic stroke. SETD5-AS1 expression in brain tissues of ischemic stroke mice and control mice was detected by quantitative Real-time-polymerase chain reaction (qRT-PCR). Proliferation and apoptosis of N2a cells were detected after transfection of overexpression plasmid or siRNA SETD5-AS1. The downstream gene of SETP5-AS1 was predicted by Starbase and PTEN was screened out. Both mRNA and protein expressions of PTEN in MCAO model and OGD/R model were detected. Furthermore, the binding condition of SETD5-AS1 and PTEN was verified by dual-luciferase reporter gene assay, RNA pull-down assay and RNA binding protein immunoprecipitation (RIP). The regulatory effect of SETD5-AS1 on PI3K/AKT pathway was detected by Western blot. RESULTS: SETD5-AS1 was highly expressed in the ischemia-reperfusion injury model. Overexpression of SETD5-AS1 in N2a cells resulted in increased apoptosis and decreased proliferation. PTEN expression was upregulated in MCAO model and OGD/R model. Dual-luciferase reporter gene assay indicated that SETD5-AS1 can promote PTEN transcription. The binding condition of SETD5-AS1 and PTEN was further verified by RNA pull-down assay and RIP. Overexpression of SETD5-AS1 in N2a cells inhibited PI3K/AKT pathway. CONCLUSIONS: SETD5-AS1 is highly expressed in the ischemia-reperfusion injury model. SETD5-AS1 participates in the development of ischemic stroke by activating PTEN and inhibiting PI3K/AKT pathway.
Subject(s)
Infarction, Middle Cerebral Artery/genetics , PTEN Phosphohydrolase/genetics , PTEN Phosphohydrolase/metabolism , RNA, Long Noncoding/genetics , Stroke/genetics , Animals , Apoptosis , Cell Death , Cell Line , Cell Proliferation , Disease Models, Animal , Infarction, Middle Cerebral Artery/metabolism , Male , Mice , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction , Stroke/metabolism , Up-RegulationABSTRACT
Tissue tolerance to pelvic intraarterial chemoembolization with cisplatin-lipiodol suspension was studied in rabbits. Cisplatin (3 mg/kg) was used with different doses of lipiodol (0.0, 0.1, 0.2, and 0.3 ml/kg). Cisplatin-lipiodol suspension was injected into the umbilical artery through a long polyethylene catheter. Local tissue concentration of platinum was increased with lipiodol, while that in the liver, heart, and kidneys was reduced. Tissue retention of platinum was linearly related to the dosage of lipiodol. With a single dose of 0.2 ml/kg lipiodol, only slight degeneration and sparse hemorrhage were observed without necrosis.
