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Tannic Acid: a Possible Therapeutic Agent for Hypermethioninemia-Induced Neurochemical Changes in Young Rats

Bernardo de Moraes Meine,Julia Eisenhardt de Mello, Solange Vega Custódio, Larissa Menezes da Silveira, William Sanabria Simões,Natália Pontes Bona,Driele Neske Garcia,Augusto Schneider, Lucas Petitemberte de Souza,William Borges Domingues,Vinicius Farias Campos,Roselia Maria Spanevello,Mayara Sandrielly Soares de Aguiar, Francieli Moro Stefanello

Biochemical and Biophysical Research Communications(2024)

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摘要
This study explores the therapeutic benefits of tannic acid (TnA) in an experimental protocol of chronic hypermethioninemia in rats. Rats were categorized in the four groups: Group I - control, Group II - TnA 30 mg/kg, Group III - methionine (Met) 0.2–0.4 g/kg + methionine sulfoxide (MS) 0.05–0.1 g/kg, Group IV - TnA/Met+MS. Saline was administered by subcutaneous pathway into groups I and II twice daily from postnatal day 6 (P6) to P28, whereas those in groups III and IV received Met+MS. From P28 to P35, groups III and IV received TnA orally. Animals from group III presented cognitive and memory impairment assessed through object recognition and Y-maze tests (p<0.05). Elevated levels of reactive species, lipid peroxidation, and nitrites followed by a decline in sulfhydryl content, catalase activity, and superoxide dismutase activity were observed in animals treated with Met+MS (p<0.05). However, TnA treatment reversed all these effects (p<0.05). In group III, there was an increase in acetylcholinesterase activity and IL-6 levels, coupled with a reduction in Na+/K+-ATPase activity (p<0.05). TnA was able to protect against these effects (p<0.05). The gene expression of catalase, brain-derived neurotrophic factor, and nuclear factor erythroid 2-related factor 2 was decreased in the hippocampus and striatum from group III (p<0.05). TnA reversed almost all of these alterations (p<0.05). These findings suggest that TnA is a therapeutic target for patients with hypermethioninemia.
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关键词
Therapeutic,Hypermethioninemia,Oxidative stress,Gene expression,Neuroprotection
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