Author/Authors :
Yang, Shasha Chengdu University of Traditional Chinese Medicine, Sichuan province, China , Wu, Jing Guiyang College of Traditional Chinese Medicine, Guizhou province, China , Zhang, Qinxiu Department of Otorhinolaryngology - Head and Neck Surgery - Teaching Hospital of Chengdu University of Traditional Chinese Medicine - Sichuan province, China , Xinrong, Li Department of Otorhinolaryngology - Head and Neck Surgery - Teaching Hospital of Chengdu University of Traditional Chinese Medicine - Sichuan province, China , Liu, Daien Chengdu University of Traditional Chinese Medicine, Sichuan province, China , Zeng, Bin Chengdu University of Traditional Chinese Medicine, Sichuan province, China , Liu, Zhiqing Chengdu University of Traditional Chinese Medicine, Sichuan province, China , Kang, Haoran Chengdu University of Traditional Chinese Medicine, Sichuan province, China , Zhong, Zhendong Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, , China
Abstract :
Allergic rhinitis (AR) is a major concern in personal and public health, which negatively affects emotions and behavior, leading to cognitive deficits, memory decline, poor school performance, anxiety, and depression. Several cellular and molecular mediators are released in the inflammatory process of AR and activate common neuroimmune mechanisms, involving emotionally relevant circuits and the induction of anxiety. Responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis to allergic processes have been reported, which may also include responsiveness of the hippocampus, cortex, and other brain regions. Here, we have used an optimized rat model of AR to explore whether the disease has a relationship with inflammatory responses in the hippocampus. AR was established in adult rats by ovalbumin sensitization, and the expression of various inflammatory substances in the hippocampus was measured by specific assays. Comparison between experimental and various control groups of animals revealed an association of AR with significant upregulation of substance P, microglia surface antigen (CD11b), glial fibrillary acid protein (GFAP), tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) in the hippocampus. Thus, we hypothesize that the AR challenge may activate these inflammatory mediators in the hippocampus, which in turn contribute to the abnormal behavior and neurological deficits associated with AR.
Keywords :
Allergic Rhinitis , Rats , Inflammatory Response , Hippocampus