The Isolated and Combined Effects of Folic Acid and Synthetic Bioactive Compounds against Aβ(25-35)-Induced Toxicity in Human Microglial Cells

Molecules

Yih-Fong Liew¹  Chao-Tzu Huang¹  Shang-Shing P. Chou¹  Yuh-Chi Kuo¹  Shiu-Huey Chou¹  Jyh-Yih Leu¹  Woan-Fang Tzeng¹  Su-Jane Wang¹  Ming-Chi Tang¹ 

[1] ¹Department of Nutritional Science, Fu-Jen University, 510 Chung-Cheng Rd., Hsinchuang, Taipei County 242, Taiwan

关键词: folate;    Aβ_(25-35) peptide;    microglial cells;    newly synthesized compounds;    superoxide production;    nitric oxide;   

DOI  :  10.3390/molecules15031632

来源: mdpi

【 摘 要 】

Folic acid plays an important role in neuronal development. A series of newly synthesized bioactive compounds (NSCs) was reported to exhibit immunoactive and neuroprotective functions. The isolated and combined effects of folic acid and NSCs against β-amyloid (Aβ)-induced cytotoxicity are poorly understood. These effects were tested using human microglia cells (C13NJ) subjected to Aβ_(25-35) challenge. According to an MTT assay, treatment of C13NJ cells with Aβ_(25-35) at 10~100 μM for 48 h induced 18%~43% cellular death in a dose-dependent manner (p < 0.05). Aβ_(25-35) treatment at 25 μM induced nitrite oxide (NO) release, elevated superoxide production, and reduced the distribution of cells in the S phase. Preincubation of C13NJ with 100 μM folic acid protected against Aβ_(25-35)-induced cell death, which coincided with a reduction in NO release by folic acid supplements. NSC47 at a level of 50 μM protected against Aβ_(25-35)-induced cell death and reduced Aβ-promoted superoxide production (p < 0.05). Folic acid in combination with NSC47 at their cytoprotective doses did not synergistically ameliorate Aβ_(25-35)-associated NO release, superoxide production, or cell cycle arrest. Taken together, folic acid or NSC treatment alone, but not the combined regimen, protected against Aβ_(25-35)-induced cell death, which may partially, if not completely, be mediated by free radical-scavenging effects.

【 授权许可】

CC BY   
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.