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首页> 外文期刊>Gut Pathogens >The neurotoxic effects of ampicillin-associated gut bacterial imbalances compared to those of orally administered propionic acid in the etiology of persistent autistic features in rat pups: effects of various dietary regimens
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The neurotoxic effects of ampicillin-associated gut bacterial imbalances compared to those of orally administered propionic acid in the etiology of persistent autistic features in rat pups: effects of various dietary regimens

机译：与口服丙酸相比，氨苄西林相关肠道细菌失衡对大鼠幼仔持续自闭症的病因具有神经毒性：各种饮食方案的影响

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Hypothesis A healthy gut with normal intestinal microflora is completely disrupted by oral antibiotics. The byproducts of harmful gut bacteria can interfere with brain development and may contribute to autism. Strategies to improve the gut microflora profile through dietary modification may help to alleviate gut disorders in autistic patients. Method Sixty young male western albino rats were divided into six equal groups. The first group served as the control; the second group was given an oral neurotoxic dose of propionic (PPA) (250 mg/kg body weight/day) for three days. The third group received an orogastric dose of ampicillin (50 mg/kg for three weeks) with a standard diet. Groups 4, 5 and 6 were given an orogastric dose of ampicillin and fed high-carbohydrate, high-protein and high-lipid diets, respectively, for 10 weeks. Biochemical parameters related to oxidative stress were investigated in brain homogenates from each group. Result The microbiology results revealed descriptive changes in the fecal microbiota of rats treated with ampicillin either alone or with the three dietary regimens. The results of PPA acid and ampicillin treatment showed significant increases in lipid peroxidation and catalase with decreases in glutathione and potassium compared with levels in the control group. A protein-rich diet was effective at restoring the glutathione level, while the carbohydrate-rich diet recovered lipid peroxidation and catalase activity. In addition, the three dietary regimens significantly increase the potassium level in the brain tissue of the test animals. Lactate dehydrogenase was remarkably elevated in all groups relative to the control. No outstanding effects were observed in glutathione S-transferase and creatine kinase. Conclusion The changes observed in the measured parameters reflect the neurotoxic effects of PPA and ampicillin. Lipid peroxide and catalase activity and the levels of glutathione and potassium are satisfactory biomarkers of PPA and ampicillin neurotoxicity. Based on the effects of the three dietary regimens, a balanced diet can protect against PPA or ampicillin-induced neurotoxicity that might induce autistic traits. These outcomes will help efforts directed at controlling the prevalence of autism, a disorder that has recently been associated with PPA neurotoxicity.
机译：假设口服抗生素会完全破坏正常肠道菌群的健康肠道。有害肠道细菌的副产物会干扰大脑发育，并可能导致自闭症。通过饮食改良来改善肠道菌群的策略可能有助于减轻自闭症患者的肠道疾病。方法将60只雄性西部白化病雄性大鼠分成六等分。第一组为对照组;第二组为对照组。第二组给予丙酸（PPA）口服神经毒性剂量（250 mg / kg体重/天），持续三天。第三组接受标准饮食，口服胃液氨苄西林（50 mg / kg，持续三周）。第4、5和6组分别给予口服胃液氨苄西林，并分别饲喂高碳水化合物，高蛋白和高脂饮食，持续10周。在每个组的脑匀浆中研究了与氧化应激相关的生化参数。结果微生物学结果显示，单独使用氨苄西林或三种饮食方案治疗的大鼠，粪便微生物群均发生了描述性变化。与对照组相比，PPA酸和氨苄青霉素的治疗结果显示脂质过氧化和过氧化氢酶显着增加，而谷胱甘肽和钾的减少。富含蛋白质的饮食可有效恢复谷胱甘肽水平，而富含碳水化合物的饮食可恢复脂质过氧化和过氧化氢酶活性。另外，这三种饮食方案显着增加了试验动物脑组织中的钾水平。相对于对照，所有组中的乳酸脱氢酶均显着升高。在谷胱甘肽S-转移酶和肌酸激酶中未观察到显着效果。结论所测参数的变化反映了PPA和氨苄青霉素的神经毒性作用。脂质过氧化物和过氧化氢酶活性以及谷胱甘肽和钾的水平是PPA和氨苄青霉素神经毒性的令人满意的生物标志物。根据这三种饮食方案的影响，均衡饮食可以预防PPA或氨苄西林引起的可能引起自闭症特征的神经毒性。这些结果将有助于控制自闭症的流行，自闭症是最近与PPA神经毒性相关的疾病。

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