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副丙酮酸通过抑制α-酮戊二酸脱氢酶复合体诱导C57BL/6JNarl小鼠神经退行性变。

Parapyruvate Induces Neurodegeneration in C57BL/6JNarl Mice via Inhibition of the α-Ketoglutarate Dehydrogenase Complex.

作者信息

Lee Inn, Song Tuzz-Ying, Chen Chien-Lin, Yang Jiann-Jou, Yang Nae-Cherng

机构信息

Department of Nutrition, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Rd., Taichung 40201, Taiwan.

Department of Medicinal Botanicals and Foods on Health Applications, Da-Yeh University, No. 168, University Rd., Dacun, Changhua 51591, Taiwan.

出版信息

ACS Omega. 2024 Jan 25;9(5):5919-5931. doi: 10.1021/acsomega.3c09469. eCollection 2024 Feb 6.

Abstract

Parapyruvate is a substance commonly found in commercial dietary supplements of calcium pyruvate (DSCP) that inhibits the α-ketoglutarate dehydrogenase complex (KGDHC) and has been shown to induce senescence in human Hs68 cells. However, it is unknown whether parapyruvate can induce neurodegeneration. In this study, the parapyruvate content in DSCP was converted to an equivalent dose for mice and administered to the C57BL/6JNarl mice at doses around the equivalent dose for 69 days, including 5, 50, and 500 mg/kg/day. The Morris water maze (MWM) task and the active avoidance test were conducted to assess the learning and memory ability in mice, and then brain tissues were collected for biochemical analyses. The results demonstrated that parapyruvate significantly impaired the learning and memory ability, decreased the KGDHC activity, and promoted the oxidative stress and acetylcholinesterase (AChE) activity in mice in a dose-dependent manner. Additionally, parapyruvate induced Tau and phosphorylated Tau (p-Tau) aggregation at dosages ≥5 mg/kg/day and increased the myelin basic protein (MBP) expression at a dosage of 500 mg/kg/day. These results suggest that the equivalent dose of parapyruvate can induce neurodegeneration in the C57BL/6JNarl mice.

摘要

副丙酮酸是一种常见于丙酮酸钙商业膳食补充剂(DSCP)中的物质,它会抑制α-酮戊二酸脱氢酶复合体(KGDHC),并且已被证明能在人Hs68细胞中诱导衰老。然而,尚不清楚副丙酮酸是否会诱发神经退行性变。在本研究中,将DSCP中的副丙酮酸含量换算成小鼠的等效剂量,并以约等效剂量的剂量给予C57BL/6JNarl小鼠69天,剂量包括5、50和500毫克/千克/天。进行了莫里斯水迷宫(MWM)任务和主动回避试验以评估小鼠的学习和记忆能力,然后收集脑组织进行生化分析。结果表明,副丙酮酸以剂量依赖性方式显著损害小鼠的学习和记忆能力,降低KGDHC活性,并促进氧化应激和乙酰胆碱酯酶(AChE)活性。此外,副丙酮酸在剂量≥5毫克/千克/天时诱导Tau和磷酸化Tau(p-Tau)聚集,并在剂量为500毫克/千克/天时增加髓鞘碱性蛋白(MBP)表达。这些结果表明,副丙酮酸的等效剂量可在C57BL/6JNarl小鼠中诱发神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4814/10851423/77be6a2d7ce0/ao3c09469_0001.jpg

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