Ukkirapandian Kavitha, E Kayalvizhi, Udaykumar Karthika Priyadharshini, Kandhi Suganya, R Muthulakshmi
Physiology, Meenakshi Medical College Hospital and Research Institute, Meenakshi Academy of Higher Education and Research (MAHER) University, Chennai, IND.
Physiology, Sri Venkateshwaraa Medical College Hospital and Research Centre, Pondicherry, IND.
Cureus. 2022 Sep 28;14(9):e29717. doi: 10.7759/cureus.29717. eCollection 2022 Sep.
Introduction Autism spectrum disorder (ASD) is a neurodevelopmental disorder, and a tremendous increase in the incidence of autism poses challenges in identifying the different treatment modalities. Since the defined etiology, pathophysiology, and treatment of autism are unavailable, translational research is being done by creating animal models of autism. This study aimed to assess the effects of on developmental and histopathological changes in autism-induced Wistar rats. Materials and methods A rat model of autism was created by administering sodium valproate on the 12th day of pregnancy, and rat pups of this group were considered autism-induced. Rat pups of pregnant rats who had received normal saline on the 12th day of pregnancy were considered group I (negative control group). Neural reflexes were assessed in early postnatal days (PND) to confirm the development of autism. Autism-induced rat pups were divided into the following two groups: group II, autism (positive control group), and group III, autism + (drug-treated group). On the 21st postnatal day (PND), group III was given an ethanolic extract of (200 mg/kg), and group I and group II were given normal saline orally for 15 days. After 15 days of drug exposure, at 36thPND, the rats were sacrificed, and brain tissue was collected for histopathological analysis. Results When compared to the negative control group, autism-induced rat pups showed delayed appearance of neurological reflexes. Neurodegenerative changes were well appreciated in group II (autism-induced rats) than in group III (autism + ). In the histomorphometric analysis, group II showed a significant reduction in the number of neurons in the frontal cortex and Purkinje cells in the cerebellum. However, when compared to group II, group III (autism treated with s) did not show significant alteration. Conclusion Valproate exposure at mid-pregnancy creates autism by disturbing neural structures among rat pups. This was clinically represented as the delayed appearance of neural reflexes. in the early postnatal period protects rat pups' brain morphology against autism pathology.
引言
自闭症谱系障碍（ASD）是一种神经发育障碍，自闭症发病率的大幅上升对确定不同的治疗方式构成了挑战。由于自闭症的明确病因、病理生理学和治疗方法尚不清楚，因此正在通过创建自闭症动物模型来进行转化研究。本研究旨在评估[具体药物名称未给出]对自闭症诱导的Wistar大鼠发育和组织病理学变化的影响。
材料与方法
在怀孕第12天给予丙戊酸钠创建自闭症大鼠模型，该组大鼠幼崽被视为自闭症诱导组。怀孕大鼠在怀孕第12天接受生理盐水的大鼠幼崽被视为第一组（阴性对照组）。在出生后早期（PND）评估神经反射以确认自闭症的发展。自闭症诱导的大鼠幼崽分为以下两组：第二组，自闭症组（阳性对照组），和第三组，自闭症 + [具体药物名称未给出]组（药物治疗组）。在出生后第21天（PND），第三组给予[具体药物名称未给出]的乙醇提取物（200mg/kg），第一组和第二组口服生理盐水，持续15天。药物暴露15天后，在第36天PND时，处死大鼠，收集脑组织进行组织病理学分析。
结果
与阴性对照组相比，自闭症诱导的大鼠幼崽神经反射出现延迟。第二组（自闭症诱导大鼠）的神经退行性变化比第三组（自闭症 + [具体药物名称未给出]组）更明显。在组织形态计量分析中，第二组额叶皮质神经元数量和小脑浦肯野细胞数量显著减少。然而，与第二组相比，第三组（用[具体药物名称未给出]治疗的自闭症组）没有显示出显著变化。
结论
孕期中期暴露于丙戊酸钠会通过干扰大鼠幼崽的神经结构而导致自闭症。这在临床上表现为神经反射出现延迟。出生后早期给予[具体药物名称未给出]可保护大鼠幼崽的脑形态免受自闭症病理影响。
