Effect of Yi-nao-jie-yu decoction on γ-aminobutyric acid type A receptor in the hippocampus and serum inflammatory factors in a rat model of poststroke anxiety.
Effect of Yi-nao-jie-yu decoction on γ-aminobutyric acid type A receptor in the hippocampus and serum inflammatory factors in a rat model of poststroke anxiety.
复制标题
益脑解郁汤对脑卒中后焦虑模型大鼠海马γ-氨基丁酸A型受体及血清炎症因子的影响
DOI：
10.2147/ndt.s115116
复制
发表时间：
2016
影响因子：
3.2
通讯作者：
Tang Q
中科院分区：
文献类型：
--
作者：
Zhang W;Zhao R;Li X;Cui X;Zhao Z;Mao Y;Wu F;Tang Q
益脑解郁汤（YNJYD）是一种广泛应用于中医临床的中药制剂，近年来已成为治疗中风后焦虑症（PSA）的重要新药。神经内分泌-免疫系统在PSA机制中起重要作用，尽管YNJYD的调节作用尚不清楚。本研究探讨了YNJYD对PSA大鼠模型神经内分泌免疫系统的潜在影响。通过右侧苍白球注射VII型胶原酶并辅以空水瓶刺激2周建立PSA模型。假手术组和PSA模型组灌胃生理盐水，治疗组灌胃丁螺环酮（BuSpar）或养阴解毒汤。每周一次采用旷场实验和高架十字迷宫进行行为学评价。苏木精-伊红染色观察病理变化。放射免疫法检测血清肿瘤坏死因子、白细胞介素（IL）-6、促肾上腺皮质激素、促甲状腺激素、游离三碘甲状腺原氨酸、游离甲状腺素、IL-1α和皮质醇水平。Western blot和实时荧光定量PCR检测γ-氨基丁酸A型受体（GABAAR）α2亚基的表达。在旷场试验和高架十字迷宫中，YNJYD治疗组大鼠在21天和28天时的恢复明显优于BuSpar治疗组大鼠。苏木精-伊红染色显示治疗组海马神经修复。饮脑愈疡汤组血清IL-1α水平明显低于模型组和BuSpar组。PSA模型组GABAAR蛋白和mRNA表达均高于假手术组，而饮脑降压汤可逆转PSA模型组GABAAR蛋白和mRNA的表达。养脑健脑饮主要通过降低海马IL-1α水平和下调GABAAR表达，维持神经内分泌-免疫系统平衡，减轻PSA症状。
The Yi-nao-jie-yu decoction (YNJYD) is a herbal preparation widely used in the clinics of traditional Chinese medicine and has been recently used as an important new therapeutic agent in poststroke anxiety (PSA). The neuroendocrine–immune system plays an important role in PSA mechanisms, although the modulating effects of YNJYD remain unknown. This study investigated the potential effects of YNJYD on the neuroendocrine–immune system in a rat model of PSA. The PSA model was induced by injecting collagenase (type VII) into the right globus pallidus, accompanied by empty water bottle stimulation for 2 weeks. The sham group and the PSA model group were gavaged with saline, while the treatment groups received buspirone (BuSpar) or YNJYD. Behavior was evaluated with the open field test and elevated plus maze once a week. Pathological changes were observed by hematoxylin and eosin staining. Serum levels of tumor necrosis factor, interleukin (IL)-6, adrenocorticotropic hormone, thyroid stimulating hormone, free triiodothyronine, free thyroxine, IL-1α, and cortisol were detected by radioimmunoassay. Expression of the γ-aminobutyric acid type A receptor (GABAAR) α2 subunit was examined by Western blot and real-time polymerase chain reaction. YNJYD-treated rats exhibited significantly better recovery than BuSpar-treated rats at 21 days and 28 days in the open field test and elevated plus maze. Hematoxylin and eosin staining revealed neural repair in the hippocampus in the treatment groups. Serum levels of IL-1α in the YNJYD group were significantly less than those in the model group and the BuSpar group. GABAAR protein and mRNA expressions were higher in the PSA model group than in the sham group, and YNJYD reversed these effects. YNJYD alleviated the symptoms of PSA mainly by decreasing IL-1α levels and downregulating GABAAR expression in the hippocampus to maintain a neuroendocrine–mmune system balance.