Raw and processed data supporting "Human chorionic gonadotropin decreases cerebral cystic encephalomalacia and parvalbumin interneuron degeneration in a pro-inflammatory model of mouse neonatal hypoxia-ischemia"
Description
This dataset contains histological, immunohistochemical, quantitative, and image data supporting the publication “Human chorionic gonadotropin decreases cerebral cystic encephalomalacia and parvalbumin interneuron degeneration in a pro-inflammatory model of mouse neonatal hypoxia-ischemia” in Scientific Reports. Data were generated using a lipopolysaccharide (LPS)-sensitized neonatal mouse model of hypoxia-ischemia (HI), with and without human chorionic gonadotropin (hCG) pretreatment. The dataset includes measurements of tissue loss and cystic encephalomalacia, assessments of parvalbumin (PV) interneuron integrity, and quantification of microglial Iba1 immunoreactivity, along with corresponding high-resolution histological and immunofluorescence images acquired using a NanoZoomer slide scanner. The dataset comprises raw and processed quantitative data files (CSV), high-resolution image files (TIF), and accompanying documentation organized to support reproducibility and reuse. Folder and file organization is designed to align with figures and supplemental figures in the associated publication.
Files
Steps to reproduce
Neonatal hypoxia-ischemia was induced in postnatal day 8 (P8) C57BL/6J mice using an LPS-sensitized model, as described in the Methods section of the associated manuscript. Mice received intraperitoneal human chorionic gonadotropin (hCG, 1.5 IU/g) or saline vehicle 2 hours prior to intraperitoneal lipopolysaccharide (LPS, Escherichia coli O55:B5, 0.6 µg/g). Eighteen hours after LPS injection, hypoxia-ischemia was induced by permanent cauterization of the left carotid artery under isoflurane anesthesia, followed by exposure to 8% oxygen for 20 minutes at 36.5 °C. Animals were euthanized at postnatal day 16 and perfused with phosphate-buffered saline. Brains were fixed in 4% paraformaldehyde, cryoprotected in 30% sucrose, and coronally sectioned at 50 µm. Tissue injury was assessed using cresyl violet staining. Immunohistochemistry was performed on free-floating sections for parvalbumin (PV) and the microglial marker Iba1. Sections were digitally scanned using a Hamamatsu NanoZoomer 2.0. Quantitative analysis was conducted using NDP.view2 and ImageJ software with bilateral regions of interest defined in cortex, striatum, and hippocampus. Tissue loss was calculated by comparing injured and contralateral hemispheres. PV immunoreactivity was quantified as percent area in cortex and by cell counts in striatum and hippocampus. All analyses were performed blinded to treatment condition. Statistical analyses were conducted using GraphPad Prism 9 with normality testing and appropriate parametric or non-parametric tests. Detailed experimental procedures, including animal handling, hypoxia-ischemia induction, dosing and timing of hCG and LPS administration, tissue processing, immunohistochemistry protocols, image acquisition, quantitative analysis, and statistical methods, are fully described in the Methods section of the associated manuscript: Human chorionic gonadotropin decreases cerebral cystic encephalomalacia and parvalbumin interneuron degeneration in a pro-inflammatory model of mouse neonatal hypoxia-ischemia.
Institutions
- Washington University in St. LouisMO, Saint Louis
Categories
Funders
- National Institute of Neurological Disorders and StrokeNational Institutes of HealthUnited StatesGrant ID: R01NS112234
- Hope Center for Neurological DisordersUnited States
Additional Metadata for Digital Commons Data@Becker
| Keywords | Lipopolysaccharides, LPS, hCG, Parvalbumins, GABAergic Neurons, Neuroprotection, Encephalomalacia, Cystic Degeneration, Microglia, Iba1, AIF-1, Neuroinflammation, Neonatal Brain Injury, Human Chorionic Gonadotropin, Hypoxia-Ischemia |
| Other Contributing Institutions | Washington University Medical Center |