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Neuroprotective Potentials of Berberine in Rotenone-Induced Parkinson's Disease-like Motor Symptoms in Rats.
Tseng, Hsiang-Chien; Wang, Mao-Hsien; Fang, Chih-Hsiang; Lin, Yi-Wen; Soung, Hung-Sheng.
Afiliação
  • Tseng HC; Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 11101, Taiwan.
  • Wang MH; School of Medicine, Fu Jen Catholic University, New Taipei City 24205, Taiwan.
  • Fang CH; Department of Anesthesia, En Chu Kon Hospital, Sanshia District, New Taipei City 23702, Taiwan.
  • Lin YW; Department of Orthopedics, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
  • Soung HS; Institute of Biomedical Engineering, National Taiwan University, Taipei 10051, Taiwan.
Brain Sci ; 14(6)2024 Jun 13.
Article em En | MEDLINE | ID: mdl-38928596
ABSTRACT
Rotenone (RTN) induces neurotoxicity and motor dysfunction in rats, mirroring the pathophysiological traits of Parkinson's disease (PD), including striatal oxidative stress, mitochondrial dysfunction, and changes in neural structure. This makes RTN a valuable model for PD research. Berberine (BBR), an isoquinoline alkaloid recognized for its antioxidative, anti-inflammatory, and neuroprotective properties, was evaluated for its ability to counteract RTN-induced impairments. Rats received subcutaneous RTN at 0.5 mg/kg for 21 days, resulting in weight loss and significant motor deficits assessed through open-field, bar catalepsy, beam-crossing, rotarod, and grip strength tests. BBR, administered orally at 30 or 100 mg/kg doses, one hour prior to RTN exposure for the same duration, effectively mitigated many of the RTN-induced motor impairments. Furthermore, BBR treatment reduced RTN-induced nitric oxide (NO) and lipid peroxidation (LPO) levels, bolstered antioxidative capacity, enhanced mitochondrial enzyme activities (e.g., succinate dehydrogenase (SDH), ATPase, and the electron transport chain (ETC)), and diminished striatal neuroinflammation and apoptosis markers. Notably, the co-administration of trigonelline (TGN), an inhibitor of the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway, significantly attenuated BBR's protective effects, indicating that BBR's neuroprotective actions are mediated via the Nrf2 pathway. These results underscore BBR's potential in ameliorating motor impairments akin to PD, suggesting its promise in potentially delaying or managing PD symptoms. Further research is warranted to translate these preclinical findings into clinical settings, enhancing our comprehension of BBR's therapeutic prospects in PD.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article