Journal: bioRxiv
Article Title: Chronic Paraventricular OX1R Overexpression Induces Oxidative Stress and Hypertension in Rats
doi: 10.64898/2026.02.09.704927
Figure Lengend Snippet: Primary neuronal cultures derived from neonatal Sprague–Dawley rats were infected with either AAV2-OX1R or control virus (AAV2-GFP). Five days post-infection, cells were treated with orexin A or vehicle for 6 hours before quantitative PCR (qPCR) analysis. Fluorescent imaging confirmed reporter gene expression in AAV-OX1R–infected neurons, indicating successful viral transduction. Graphs summarize the effects of OX1R overexpression, with or without orexin A treatment, on the expression of Cyba, Cybb, SOD1, SOD2, and neuronal activation markers Jun and Fosl1. In OX1R-overexpressing neurons, basal SOD1 expression was reduced by ∼30% (*P<0.05), while other oxidative stress–related genes remained unchanged. Upon orexin A stimulation, SOD2 expression was significantly decreased by ∼35%, whereas CYBB (1.7-fold), Jun (4-fold), and Fosl1 (7-fold) were markedly upregulated (n=4 per group, *P<0.05) compared to control AAV-GFP infection neurons. Data are presented as mean ± SEM, and statistical analyses were performed using Student’s t-test. Scale bar: 100 µm.
Article Snippet: Adult male Sprague–Dawley rats received bilateral PVN injections of AAV2-OX1R or control virus AAV2-GFP.
Techniques: Derivative Assay, Infection, Control, Virus, Real-time Polymerase Chain Reaction, Imaging, Gene Expression, Transduction, Over Expression, Expressing, Activation Assay