<br>天麻多糖通过抑制细胞凋亡和炎症信号通路以及调节肠道微生物群缓解帕金森病,Food & Function

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天麻多糖通过抑制细胞凋亡和炎症信号通路以及调节肠道微生物群缓解帕金森病
Food & Function ( IF 5.1 ) Pub Date : 2024-02-22 , DOI: 10.1039/d3fo05169b
Qing-Xia Gan _{1,

2} , Mao-Yao Peng _{1,

2} , Hao-Bo Wei _{1,

2} , Lin-Lin Chen _{1,

2} , Xiao-Yan Chen _{1,

2} , Zi-Han Li _{1,

2} , Guang-Qin An _{1,

2} , Yun-Tong Ma _{1,

2}

Affiliation

帕金森病（PD）是一种常见的、慢性的、进行性的中枢神经系统退行性疾病，目前尚无有效的治疗方法。天麻是一种著名的食药同源资源，具有神经保护潜力。天麻多糖（GEP）是天麻中高活性、安全的成分，是功能性产品开发的重要成分。在这项研究中，GEP 被给予 1-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 诱导的小鼠 3 周以上，以研究其神经保护作用。结果表明，GEP显着缓解PD小鼠的运动功能障碍，抑制α-突触核蛋白的积累，减少大脑中多巴胺能神经元的损失。此外，GEP 增加了 Bcl-2/Bax 比率并降低了 cleaved-caspase-3 水平，表明 GEP 可能通过阻止 MPTP 诱导的线粒体凋亡来改善 PD。 GEP还能显着抑制PD小鼠脑内GFAP的增加，降低TNF-α、IL-1β、IL-6的水平，这可能是通过灭活TLR4/NF抑制神经炎症的结果-κB途径。此外，GEP的神经保护作用涉及肠脑轴，研究表明GEP可调节与PD相关的肠道微生物群（如阿克曼氏菌、乳杆菌、拟杆菌、普雷沃氏菌和粪杆菌）的失调，增加微生物代谢产物SCFA的含量结肠中并增加了修复 PD 小鼠肠道屏障的 occludin 水平。综上所述，本研究有望从神经保护作用的角度为GEP功能性产品的开发和应用提供理论依据。

"点击查看英文标题和摘要"

Gastrodia elata polysaccharide alleviates Parkinson's disease via inhibiting apoptotic and inflammatory signaling pathways and modulating the gut microbiota

Parkinson's disease (PD) is a common, chronic, and progressive degenerative disease of the central nervous system for which there is no effective treatment. Gastrodia elata is a well-known food and medicine homologous resource with neuroprotective potential. Gastrodia elata polysaccharide (GEP), which is a highly active and safe component in Gastrodia elata, is an important ingredient in the development of functional products. In this study, GEP was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice over 3 weeks to investigate its neuroprotective effects. The results showed that GEP significantly alleviated the motor dysfunction of PD mice, inhibited the accumulation of α-synuclein, and reduced the loss of dopaminergic neurons in the brain. Moreover, GEP increased the Bcl-2/Bax ratio and decreased the cleaved-caspase-3 level, suggesting that GEP may ameliorate PD by preventing MPTP-induced mitochondrial apoptosis. GEP also significantly inhibited the increase of GFAP and decreased the levels of TNF-α, IL-1β, and IL-6 in the brain of PD mice, which may be the result of the inhibition of neuroinflammation by the inactivation of the TLR4/NF-κB pathway. Furthermore, the neuroprotective effects of GEP involve the gut–brain axis, as it has been shown that GEP regulated the dysbiosis of PD-related gut microbiota such as Akkermansia, Lactobacillus, Bacteroides, Prevotella, and Faecalibacterium, increased the content of microbial metabolites SCFAs in the colon and increased the level of occludin that repairs the intestinal barrier of PD mice. In conclusion, this study is expected to provide a theoretical basis for the development and application of functional products with GEP from the perspective of neuroprotective effects.

更新日期：2024-02-23

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