Dichlorvos poisoning caused chicken cerebellar autophagy and changes of Caecal microflora.

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Tác giả: Juan Chen, Shupeng Chen, Xiaona Gao, Xiaoquan Guo, Guoliang Hu, Chenxi Jiang, Huibo Jin, Lin Li, Pei Liu, Ping Liu, Salma Mbarouk Omar, Gen Wan, Ying Zhang, Yun Zhang, Yulan Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 809.008 History and description with respect to kinds of persons

Thông tin xuất bản: England : Poultry science , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 695612

In order to explore the effects of acute dichlorvos exposure on cerebellar autophagy and cecal microbes in broilers and to analyze the relationship between autophagy-related genes and cecal microbes. Broilers were randomly divided into three groups (with 16 broilers in each group)and respectively given distilled water and dichlorvos (2.48 mg / kg, 11.3 mg / kg). The cecal contents and cerebellum samples were collected after poisoning symptoms of broilers, and the antioxidant indexes such as SOD and CAT in cerebellum were detected. Hematoxylin-eosin (HE) staining of cerebellum and cecum, and immunofluorescence sections of cerebellum LC3 were made. RT-PCR and western blot were used to detect the expression of oxidative stress and autophagy-related genes in cerebellar tissue. The cecal contents were analyzed by 16S rRNA high-throughput sequencing, and then the correlation between the expression of autophagy-related genes and the abundance of intestinal microbes was analyzed. It was concluded that dichlorvos exposure destroyed the normal morphological structure of the cerebellum and cecum in broilers, which induced oxidative stress and autophagy in the cerebellum of broilers, reduced the diversity of cecal microorganisms, and destroyed the steady state of the cecal microbial structure. In addition, The changes of mRNA expression of autophagy-related genes is related to some specific bacteria. In summary, this study found that dichlorone exposure can cause cerebellar oxidative stress and autophagy, and the mechanism of cerebellar injury in broilers is linked to cecal microbiota changes, potentially offering a new direction for researching dichlorone's pathogenic mechanism.
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