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没食子酸对成年白化大鼠小脑中甲唑醇诱导的不良反应的改善作用:组织病理学和免疫组织化学证据。

Ameliorative effects of gallic acid on tebuconazole-induced adverse effects in the cerebellum of adult albino rats: histopathological and immunohistochemical evidence.

机构信息

Human Anatomy and Embryology Department, Faculty of Medicine, Assiut University, Assiut, Egypt.

出版信息

Ultrastruct Pathol. 2024 Sep 2;48(5):351-366. doi: 10.1080/01913123.2024.2387685. Epub 2024 Aug 6.

Abstract

Tebuconazole (TEB) is a common triazole sterol demethylation inhibitor fungicide utilized to manage a variety of diseases in crops like cereals, fruits, and vegetables. The aim of this work was to assess the effects of TEB on the structure of the cerebellum in adult albino rats and possible protective impact of co-administration of Gallic acid (GA). Four groups of forty adult male albino rats were randomly selected, and the rats in group I received corn oil through daily gavage for 4 weeks. Group II received GA dissolved in the normal saline at a dose of 100 mg/kg through daily gavage for 4 weeks, group III administered with TEB dissolved in corn oil at its acceptable daily intake dose (0.02 mg/kg body weight) through daily gavage for 4 weeks, group IV rats received both TEB and GA. For light microscopic, ultrastructural, and immunohistochemical investigations, cerebellar specimens were prepared. TEB exposure led to neuronal damage in the form of degenerated Purkinje cells with vacuolated cytoplasm, areas of lost Purkinje cells, the basket cells appeared vacuolated with degenerated neuropil, the granule cells clumped with congested areas between them, dilated cerebellar islands, weak positive bcl2 immunoreactions in the Purkinje cells, and numerous GFAP-positive astrocytes. GA mitigated TEB-mediated histological changes in the cerebellar cortex. We concluded that TEB caused Purkinje neurons in the rat cerebellar cortex to degenerate and undergo apoptosis. GA had a neuroprotective benefit against TEB toxicity in the rat cerebellar cortex.

摘要

戊唑醇(TEB)是一种常见的三唑固醇脱甲基抑制剂类杀菌剂,用于防治谷物、水果和蔬菜等作物的多种疾病。本研究旨在评估 TEB 对成年白化大鼠小脑结构的影响,以及同时给予没食子酸(GA)的可能保护作用。随机选择了四组四十只成年雄性白化大鼠,第 I 组通过每日灌胃给予玉米油,连续 4 周;第 II 组通过每日灌胃给予溶于生理盐水的 GA(剂量为 100mg/kg),连续 4 周;第 III 组通过每日灌胃给予溶于玉米油的 TEB(其可接受的日摄入量剂量为 0.02mg/kg 体重),连续 4 周;第 IV 组大鼠同时给予 TEB 和 GA。为了进行光镜、超微结构和免疫组织化学研究,制备了小脑标本。TEB 暴露导致神经元损伤,表现为细胞质空泡化的变性浦肯野细胞、丢失浦肯野细胞的区域、出现空泡化的 basket 细胞与变性神经毡、颗粒细胞簇集并有充血区域、扩张的小脑岛、浦肯野细胞 bcl2 免疫反应减弱以及大量 GFAP 阳性星形胶质细胞。GA 减轻了 TEB 介导的小脑皮质组织学变化。我们得出结论,TEB 导致大鼠小脑皮质浦肯野神经元变性和凋亡。GA 对 TEB 毒性具有神经保护作用。

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