详细信息
Banxia Baizhu Tianma Decoction alleviates pentylenetetrazol-induced epileptic seizures in rats by preventing neuronal cell damage and apoptosis and altering serum and urine metabolic profiles ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Banxia Baizhu Tianma Decoction alleviates pentylenetetrazol-induced epileptic seizures in rats by preventing neuronal cell damage and apoptosis and altering serum and urine metabolic profiles
作者:Gao, Lv[1,2,3];Xie, Ran[1];Yang, Xiujuan[4];Liu, Yuling[1];Lin, Rong[4];Yao, Zhengyu[2];Wang, Yingxuan[2];Dou, Baokai[1,5];Meng, Jing[1];Hu, Xiaoyu[1];Song, Lixia[1];Cheng, Jinlai[1];Shi, Zhenggang[4];Huo, Hairu[1];Sui, Feng[1];Song, Qi[1,6]
第一作者:Gao, Lv
通信作者:Huo, HR[1];Sui, F[1];Song, Q[1];Shi, ZG[2]
机构:[1]China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China;[2]Shanxi Univ Tradit Chinese Med, Taiyuan 030024, Peoples R China;[3]Shanxi Integrated Tradit Chinese & Western Med Hos, Taiyuan 030013, Peoples R China;[4]Gansu Univ Tradit Chinese Med, Lanzhou 730000, Peoples R China;[5]Shandong First Med Univ, Shandong Prov Hosp, Dept Pharm, Jinan 250021, Peoples R China;[6]Hebei Univ, Coll Tradit Chinese Med, Baoding 071000, Peoples R China
第一机构:China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China
通信机构:[1]corresponding author), China Acad Chinese Med Sci, Inst Chinese Mat Med, Beijing 100700, Peoples R China;[2]corresponding author), Gansu Univ Tradit Chinese Med, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;
年份:2025
卷号:338
外文期刊名:JOURNAL OF ETHNOPHARMACOLOGY
收录:;Scopus(收录号:2-s2.0-85210057889);WOS:【SCI-EXPANDED(收录号:WOS:001370774700001)】;
基金:This work was supported by grants from the National Natural Science Foundation of China (Grant No. 82305318, 82173998, 82374057, 82174101, 82374160), Innovation Project of the Chinese Academy of Traditional Chinese Medicine (No.CI2021A03803) and Shanxi University of Traditional Chinese Medicine Rewards Research Start-up Fund Project for Outstanding PhD Graduates coming to work in Shanxi (2021BKS06).
语种:英文
外文关键词:Banxia Baizhu Tianma decoction; Epilepsy; Urine metabolomics; Serum metabolomics; Anti-apoptosis
摘要:Ethnopharmacological relevance: Epilepsy (EP) is one of the most prevalent chronic neurological disorders in children, characterised by a prolonged course and a propensity for recurrence. Banxia Baizhu Tianma Decoction (BBTD), a traditional Chinese medicine formula, is commonly employed in the clinical management of EP and has demonstrated satisfactory therapeutic effects. Aim of the study: This study aimed to evaluate the anti-epileptic effects of BBTD and to explore its molecular mechanisms. Materials and methods: EP rat model was induced by pentylenetetrazol (PTZ) and treated with BBTD. Parameters such as seizure grade and duration were recorded to evaluate the improvement of BBTD on epileptic behavior. Nissl staining was used to observe the pathological changes in the cerebral motor cortex. The expression levels of the Bax and Bcl-2 in the motor cortex were measured by western blot analysis to assess neuronal damage and apoptosis. The therapeutic action of BBTD was evaluated by examining the levels of neurotransmitters gamma-aminobutyric acid (GABA) and glutamate (Glu) in the brain tissue of EP rats, along with assessments of neuronal damage and apoptosis. Non-targeted metabolomics techniques were employed to conduct a comprehensive analysis of serum and urine metabolites, and network analysis of metabolite-related targets was performed to enhance understanding of the anti-epileptic effects and mechanisms of BBTD. Results: After BBTD treatment, the EP model rats exhibited reduced seizure severity and shortened seizure duration. Moreover, BBTD mitigated PTZ-induced neuronal damage, as evidenced by a significant increase in the number of Nissl bodies in the motor cortex following treatment. At the same time, BBTD inhibited neuronal apoptosis, as demonstrated by the up-regulation of the anti-apoptotic protein Bcl-2 and down-regulation of the pro-apoptotic protein Bax in the brain tissue of treated rats. In addition, BBTD reversed the decreased levels of GABA and the increased levels of Glu in the brain tissue of the model group. Metabolomics analyses suggested that BBTD treatment for EP may be closely associated with alterations in urinary metabolites related to vitamin B6 and pyrimidine metabolism, as well as serum metabolites involved in purine metabolism, glycerophospholipid metabolism and vitamin B6 metabolism. Finally, network analysis of metabolite targets indicated that dopamine and alpha-linolenic acid metabolites may play significant roles in the therapeutic effects of BBTD on EP. Conclusion: BBTD demonstrated anti-epileptic effects in PTZ-induced seizure rats by regulating neurotransmitter balance, reducing neuronal damage and inhibiting apoptosis, suggesting its potential for the development of novel AEDs. This is the first time that UHPLC-MS-based urine and serum metabolomics have been used to elucidate the anti-epileptic mechanism of BBTD, providing insights into the underlying mechanisms of BBTD's action.
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