p66shc Sirna Encapsulated Nanoparticle Attenuates NMDA Induced Spasms in Prenatally Betamethasone Primed Rats
Abstract number :
1.052
Submission category :
1. Basic Mechanisms / 1D. Mechanisms of Therapeutic Interventions
Year :
2022
Submission ID :
2203918
Source :
www.aesnet.org
Presentation date :
12/3/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:22 AM
Authors :
Joon Won Kang, MD, PhD. – Chungnam National University and Hospital; University of Nebraska Medical Center; Hyeok Hee kwon, Master – Chungnam National University; Hyewon Park, Master – Chungnam National University; Hyo Jung Shin, PhD. – Chungnam National University; Seung Yeon Jung, MD – Chungnam National University Hospital; Dong Woon Kim, PhD. – Chungnam National University
Rationale: Oxidative stress can influence the central nervous system of offspring. Oxidative damage can lead to brain development disorders due to prenatal stress. Various factors, including p66Shc, regulate reactive oxygen species (ROS) generation from mitochondria. This study investigated the relationship between prenatal stress and p66Shc on N-methyl-D-aspartate (NMDA)-induced spasms.
Methods: We used pregnant female Sprague-Dawley rats and induced prenatal stress with betamethasone injection on a gestational day 15. On a postnatal day 15, NMDA was administered to trigger spasms in offspring. The p66Shc siRNA encapsulated nanoparticle was injected into the rat's brain 3 or 7 days before NMDA administration. The total number of spasms was recorded. We also measured oxidative stress in the cortex.
Results: P66Shc was highly expressed in rats prenatally stressed by betamethasone. ROS and mtROS were increased in prenatally betamethasone primed rats. We observed that rats treated with p66Shc siRNA encapsulated nanoparticle while exposed to prenatal stress demonstrated a reduced total number of spasms (p< 0.001). The effect of p66Shc siRNA encapsulated nanoparticles were similar between 3 days and 7 days before NMDA administration.
Basic Mechanisms