Tsao Shu-Ping, Nurrahma Bira Arumndari, Kumar Ravi, Wu Chieh-Hsi, Yeh Tu-Hsueh, Chiu Ching-Chi, Lee Yen-Peng, Liao Yi-Chi, Huang Cheng-Hsieh, Yeh Yao-Tsung, Huang Hui-Yu
Ph.D. Program in Drug Discovery and Development Industry, College of Pharmacy, Taipei Medical University, Taipei 11031, Taiwan.
Graduate Institute of Metabolism and Obesity Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan.
Antioxidants (Basel). 2021 Nov 17;10(11):1823. doi: 10.3390/antiox10111823.
Oxidative stress plays a key role in the degeneration of dopaminergic neurons in Parkinson's disease (PD), which may be aggravated by concomitant PD-associated gut dysbiosis. Probiotics and prebiotics are therapeutically relevant to these conditions due to their antioxidant, anti-inflammatory, and gut microbiome modulation properties. However, the mechanisms by which probiotic/prebiotic supplementation affects antioxidant capacity and the gut microbiome in PD remains poorly characterized. In this study, we assessed the effects of a AP-32 probiotic, a prebiotic (dried AP-32 culture medium supernatant), and a probiotic/prebiotic cocktail in rats with unilateral 6-hydroxydopamine (6-OHDA)-induced PD. The neuroprotective effects and levels of oxidative stress were evaluated after eight weeks of daily supplementation. Fecal microbiota composition was analyzed by fecal 16S rRNA gene sequencing. The supplements were associated with direct increases in host antioxidant enzyme activities and short-chain fatty acid production, protected dopaminergic neurons, and improved motor functions. The supplements also altered the fecal microbiota composition, and some specifically enriched commensal taxa correlated positively with superoxide dismutase, glutathione peroxidase, and catalase activity, indicating supplementation also promotes antioxidant activity via an indirect pathway. Therefore, AP-32 supplementation enhanced the activity of host antioxidant enzymes via direct and indirect modes of action in rats with 6-OHDA-induced PD.
氧化应激在帕金森病（PD）中多巴胺能神经元的退化过程中起关键作用，而PD相关的肠道生态失调可能会加剧这种退化。由于益生菌和益生元具有抗氧化、抗炎以及调节肠道微生物群的特性，它们在治疗这些病症方面具有相关性。然而，补充益生菌/益生元影响PD患者抗氧化能力和肠道微生物群的机制仍不清楚。在本研究中，我们评估了AP-32益生菌、一种益生元（干燥的AP-32培养基上清液）以及一种益生菌/益生元混合物对单侧6-羟基多巴胺（6-OHDA）诱导的PD大鼠的影响。在每日补充八周后，评估了其神经保护作用和氧化应激水平。通过粪便16S rRNA基因测序分析粪便微生物群组成。这些补充剂与宿主抗氧化酶活性和短链脂肪酸产量的直接增加相关，保护了多巴胺能神经元，并改善了运动功能。这些补充剂还改变了粪便微生物群组成，一些特定富集的共生类群与超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性呈正相关，表明补充剂也通过间接途径促进抗氧化活性。因此，在6-OHDA诱导的PD大鼠中，补充AP-32通过直接和间接作用方式增强了宿主抗氧化酶的活性。
