ArticleMetabolic brain disease2018
Therapeutic effects of probiotics on neurotoxicity induced by clindamycin and propionic acid in juvenile hamsters.
Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Impact of Aflatoxins on the Digestive, Immune, and Nervous Systems: The Role of Microbiota and Probiotics in Toxicity Protection.International journal of molecular sciences · 2025Review
- Cutibacterium Acnes induces Alzheimer's disease-like pathology in brains of wistar rats through structural changes associated with microtubules.Behavioral and brain functions : BBF · 2024Article
- Psychobiotics improve propionic acid-induced neuroinflammation in juvenile rats, rodent model of autism.Translational neuroscience · 2022Article
- The anti-inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters.Food science & nutrition · 2021Article
- Testing the combined effects of probiotics and prebiotics against neurotoxic effects of propionic acid orally administered to rat pups.Food science & nutrition · 2021Article
- The Gut Microbiota-Immunity Axis in ALS: A Role in Deciphering Disease Heterogeneity?Biomedicines · 2021Article
- Intravenous administration of sodium propionate induces antidepressant or prodepressant effect in a dose dependent manner.Scientific reports · 2020Article
- Propionate and Alzheimer's Disease.Frontiers in aging neuroscience · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study investigated the therapeutic effects of probiotics on brain intoxication induced by clindamycin and propionic acid (PPA) in hamsters. Fifty golden Syrian hamsters were randomly divided into five experimental groups of ten animals each: (A) control group receiving phosphate buffered saline; (B) oral buffered PPA-treated group being administered with a neurotoxic dose of 250 mg/kg PPA during three days; (C) oral clindamycin-treated group receiving a single dose of 30 mg clindamycin/kg; and (D, E) the two therapeutic groups being administered the same doses of clindamycin and PPA followed by probiotics for three weeks at a daily dose of 0.2 g/kg. Biochemical parameters of energy metabolism and oxidative stress were examined in brain homogenates from all hamsters. The development of pathogenic bacteria was monitored on stool samples from all hamsters. Descriptive changes in fecal microbiota and overgrowth of Clostridium species in clindamycin and PPA treated hamsters were recorded. Interestingly, probiotics were shown effective to restore normal gut microbiota. Clindamycin and PPA treatments caused an elevation in lipid peroxidation and catalase activity, as oxidative stress markers, together with a reduction in GST activity and GSH level. Energy metabolism impairment was ascertained via the activation of creatine kinase and a decrease of lactate dehydrogenase. These findings suggest that bacteria overgrowth caused by PPA and clindamycin was efficient to illustrate signs of neuronal toxicity. The present study indicates that probiotic treatment can improve poor detoxification, oxidative stress, and altered gut microbiota as mechanisms implicated in the etiology of many neurological disorders.
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