Lacto-N-fucopentaose I (LNFPI) 是一种人母乳寡糖 (HMO)，具有抗病毒和抗菌活性。Lacto-N-fucopentaose I 通过减少衣壳蛋白 VP1 来阻断病毒吸附，增加CDK2、减少cyclin E恢复细胞周期 S 期的阻滞。Lacto-N-fucopentaose I 抑制病毒感染的细胞凋亡 (apoptosis)。Lacto-N-fucopentaose I 也抑制ROS的产生。Lacto-N-fucopentaose I 还可以调节肠道菌群影响免疫系统发育。
| 生物活性 | Lacto-N-fucopentaose I (LNFPI) is a human milk oligosaccharide (HMO), possessing antiviral and antibacterial activity. Lacto-N-fucopentaose I can reduce capsid protein VP1 to block virus adsorption, promoteCDK2and reducecyclin Eto recover cell cycle S phase block. Lacto-N-fucopentaose I inhibitsROSproduction andapoptosisin virus-infected cells. Lacto-N-fucopentaose I can also regulate intestinal microbiota to affect immune system development[1]. |
| IC50& Target | Human Endogenous Metabolite | CDK2/cyclinE |
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体外研究
(In Vitro) | Lacto-N-fucopentaose I (25-3200 μg/mL;48 h) exhibits certain cytotoxicity at 3200 μg/mL but no toxic reaction below 1600 μg/mL[1].
Lacto-N-fucopentaose I (25-1600 μg/mL; 14-18 h) can protect EV71-infected RD cells from death[1].
Lacto-N-fucopentaose I (100-400 μg/mL; 16 h) decreases markedly mRNA levels of VP1 and ROS production in EV71-infected RD cells at 400 μg/mL; leads to the recovery of EV71-induced S phase arrest in RD cells[1].
Lacto-N-fucopentaose I (100 and 200 μg/mL; 3 days) inhibits cell apoptosis inCaenorhabditis elegans; significantly decreases the levels ofEgl-1,Ced-3andCed-4[1].
Lacto-N-fucopentaose I can reduce the abundance ofSphingobacterium,StenotrophomonasandAchromobacter; can increase the abundance ofMicromonospora,Vibrio,Acidibacter,Gaiella,Devosia,Steroidobacter,Variibacter,Dactylosporangium,RB41,Pir4_lineage,Pirellula,Haliangium,Roseiflexus,Pedomicrobium, andBradyrhizobium.
Cell Viability Assay[1] | Cell Line: | RD cells | | Concentration: | 25, 50, 100, 200, 400, 800, 1600 and 3200 μg/mL | | Incubation Time: | 48 h | | Result: | Exhibited certain cytotoxicity at 3200 μg/mL but no toxic reaction below 1600 μg/mL. |
RT-PCR[1] | Cell Line: | RD cells (infected with EV71) | | Concentration: | 100, 200 and 400 μg/mL | | Incubation Time: | 16 h | | Result: | Decreased markedly mRNA levels of VP1 only at 400 μg/mL. |
Apoptosis Analysis[1] | Cell Line: | RD cells (infected with EV71) | | Concentration: | 100, 200 and 400 μg/mL | | Incubation Time: | 16 h | | Result: | Decreased the rate of cells in early apoptosis to 10.9% ± 1.26% at 400 μg/mL, while the untreated EV71 group was 27.7% ± 2.13%.
Significantly inhibited the activity of caspase-3, caspase-8 and caspase-9.
Recovered the decreased mRNA expression of PAPR, NF-κB and Bcl-2 and properly regulated Bad and Fas into their normal levels. |
Cell Cycle Analysis[1] | Cell Line: | RD cells (infected with EV71) | | Concentration: | 100, 200 and 400 μg/mL | | Incubation Time: | 12 h | | Result: | Rescued EV71-induced S phase arrest, which promoted the transition of the G1 phase to the S phase. |
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| 结构分类 | - Saccharides
- Polysaccharides
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| 运输条件 | Room temperature in continental US; may vary elsewhere. |
| 储存方式 | 4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) |
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