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标题：Testing the combined effects of probiotics and prebiotics against neurotoxic effects of propionic acid orally administered to rat pups
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作者：Anwar Al Suhaibani ; Abir Ben Bacha ; Mona Alonazi 等
期刊名称：Food Science & Nutrition
电子版ISSN：2048-7177
出版年度：2021
卷号：9
期号：8
页码：4440-4451
DOI：10.1002/fsn3.2418
语种：English
出版社：John Wiley & Sons, Ltd.
摘要：The present study investigated the combined effects of mixed probiotic and bee pollen on brain intoxication induced by propionic acid (PPA) in rat pups. Thirty western albino rats were divided into five groups, six animals each: (1) Control group receiving phosphate‐buffered saline; (2) Probiotic and bee pollen‐treated group being administered at the same dose with 200 mg/kg body weight; (c) PPA‐treated group receiving a neurotoxic dose 250 mg/kg body weight of PPA for 3 days; (d) Therapeutic group being administered the neurotoxic dose of PPA followed by probiotic and bee pollen treatment 200 mg/kg body weight; (e) Protective group receiving probiotic and bee pollen mixture treatment followed by neurotoxic dose of PPA. Selected biochemical parameters linked to oxidative stress, energy metabolism, and neurotransmission were investigated in brain homogenates from all the five groups. PPA treatment showed an increase in oxidative stress markers like lipid peroxidation coupled with a significant decrease in glutathione level. Impaired energy metabolism was ascertained via the alteration of creatine kinase (CK) and lactate dehydrogenase (LDH) activities. Dramatic increase of Na+ and K+ concentrations together with a decrease of GABA and IL‐6 and an elevation of glutamate levels in PPA‐treated rat's pups confirmed the neurotoxicity effect of PPA. Interestingly, the mixed probiotic and bee pollen treatment were effective in restoring the levels of glutamate, GABA, and IL‐6 in addition to normalizing the levels of lipid peroxidation and glutathione and the activities of CK and LDH. The present study indicates that mixed probiotic and bee pollen treatment can improve poor detoxification, oxidative stress, and neuroinflammation as mechanisms implicated in the etiology of autism.