Ukkirapandian Kavitha, Elumalai Kayalvizhi, Udaykumar Karthika Priyadharshini, Vp Sundaravadivel, Rangasmy Muthulakshmi
Physiology, Meenakshi Medical College Hospital and Research Institute, Meenakshi Academy of Higher Education and Research (MAHER) University, Kanchipuram, IND.
Physiology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, IND.
Cureus. 2024 Jan 10;16(1):e52066. doi: 10.7759/cureus.52066. eCollection 2024 Jan.
Being a "behavioral disorder," autism spectrum disorder (ASD) is difficult to manage because its precise etiology is uncertain. In order to better understand the pathophysiology of autism and explore various therapeutic approaches, animal models are developed. Animal models of autism caused by valproate during pregnancy exhibit strong construct validity and reliability. Hence, this study was done among autism-induced rats with the aim of identifying the behavioral and biochemical assays. Pregnant rats were administered sodium valproate on the 12th day of gestation, while control pregnant rats received normal saline. The rats' offspring that received normal saline during intrauterine life were grouped as control, and the rats' offspring that received valproate were grouped as autism-induced. From postnatal day (PND) 21, behavioral assessments were done by using the Y maze (repetitive behavior) and the T maze (social behavior). The estimation of antioxidant profile (malondialdehyde {MDA}, glutathione {GSH}, catalase (CAT), and superoxide dismutase {SOD}), proinflammatory markers (tumor necrosis factor {TNF} alpha, transforming growth factor {TGF} beta, interleukin {IL} 6, and IL-1 beta), neurotransmitters (gamma-aminobutyric acid {GABA} and serotonin), and brain-derived neurotrophic factor (BDNF) in the hippocampal region was done. Oxidative stress, increased proinflammatory markers, and increased serotonin were recorded in the autism group. Rats with autism had a significant decrease in GABA and BDNF levels. These biochemical alterations can be correlated with clinical features of autism to diagnose and manage the disorder at the earliest.
作为一种“行为障碍”，自闭症谱系障碍（ASD）难以管理，因为其确切病因尚不确定。为了更好地理解自闭症的病理生理学并探索各种治疗方法，人们开发了动物模型。孕期丙戊酸盐所致自闭症的动物模型具有很强的结构效度和可靠性。因此，本研究以自闭症诱导大鼠为对象，旨在确定行为和生化检测方法。妊娠第12天给孕鼠注射丙戊酸钠，而对照孕鼠注射生理盐水。子宫内生活期间接受生理盐水的大鼠后代被归为对照组，接受丙戊酸盐的大鼠后代被归为自闭症诱导组。从出生后第21天起，通过Y迷宫（重复行为）和T迷宫（社交行为）进行行为评估。对海马区的抗氧化指标（丙二醛{MDA}、谷胱甘肽{GSH}、过氧化氢酶{CAT}和超氧化物歧化酶{SOD}）、促炎标志物（肿瘤坏死因子{TNF}α、转化生长因子{TGF}β、白细胞介素{IL}6和IL-1β）、神经递质（γ-氨基丁酸{GABA}和血清素）以及脑源性神经营养因子（BDNF）进行了测定。自闭症组出现氧化应激、促炎标志物增加和血清素增加。自闭症大鼠的GABA和BDNF水平显著降低。这些生化改变可与自闭症的临床特征相关联，以便尽早诊断和管理该疾病。
