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培哚普利可改善丙戊酸钠诱导的自闭症大鼠模型：涉及 Sirtuin-1、JAK2/STAT3 轴、PI3K/Akt/GSK-3β 通路和 PPAR-γ 信号。

Perindopril Ameliorates Sodium Valproate-Induced Rat Model of Autism: Involvement of Sirtuin-1, JAK2/STAT3 Axis, PI3K/Akt/GSK-3β Pathway, and PPAR-Gamma Signaling.

机构信息

Department of Pharmaceutical Sciences, College of Pharmacy, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.

Department of Pharmacology, Faculty of Medicine, Tanta University, Tanta 31527, Egypt.

出版信息

Medicina (Kaunas). 2024 Nov 3;60(11):1802. doi: 10.3390/medicina60111802.

DOI:10.3390/medicina60111802
PMID:39596986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11596946/
Abstract

Autism is a developmental disability characterized by impairment of motor functions and social communication together with the development of repetitive or stereotyped behaviors. Neither the exact etiology or the curative treatment of autism are yet completely explored. The goals of this study were to evaluate the possible effects of perindopril on a rat model of autism and to elucidate the possible molecular mechanisms that may contribute to these effects. In a rat model of sodium valproate (VPA)-induced autism, the effect of postnatal administration of different doses of perindopril on growth and motor development, social and repetitive behaviors, sirtuin-1, oxidative stress and inflammatory markers, PI3K/Akt/GSK-3β pathway, JAK2/STAT3 axis, and PPAR-gamma signaling in the hippocampal tissues were investigated. The histopathological and electron microscopic changes elicited by administration of the different treatments were also investigated. : Perindopril dose-dependently combatted the effects of prenatal exposure to VPA on growth and maturation, motor development, and social and repetitive behaviors. In addition, the different doses of perindopril ameliorated the effects of prenatal exposure to VPA on sirtuin-1, oxidative stress and inflammatory markers, PI3K/Akt/GSK-3β pathway, JAK2/STAT3 axis, and PPAR-gamma signaling. These effects had a mitigating impact on VPA-induced histopathological and electron microscopic changes in the hippocampal tissues. : Perindopril may emerge as a promising agent for amelioration of the pathologic changes of autism spectrum disorders.

摘要

自闭症是一种发育障碍，其特征是运动功能和社会交流受损，同时伴有重复或刻板行为的发展。自闭症的确切病因和治疗方法尚未完全探索。本研究的目的是评估培哚普利对自闭症大鼠模型的可能影响，并阐明可能有助于这些影响的可能分子机制。在丙戊酸钠（VPA）诱导的自闭症大鼠模型中，研究了不同剂量培哚普利在出生后给药对生长和运动发育、社会和重复行为、沉默调节蛋白-1（SIRT1）、氧化应激和炎症标志物、PI3K/Akt/GSK-3β 通路、JAK2/STAT3 轴和海马组织中过氧化物酶体增殖物激活受体-γ（PPAR-γ）信号的影响。还研究了不同治疗方法引起的组织学和电子显微镜变化。结果：培哚普利剂量依赖性地对抗了产前暴露于 VPA 对生长和成熟、运动发育以及社会和重复行为的影响。此外，不同剂量的培哚普利改善了产前暴露于 VPA 对 SIRT1、氧化应激和炎症标志物、PI3K/Akt/GSK-3β 通路、JAK2/STAT3 轴和 PPAR-γ 信号的影响。这些影响减轻了 VPA 诱导的海马组织的组织病理学和电子显微镜变化。结论：培哚普利可能成为改善自闭症谱系障碍病理变化的有前途的药物。

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