What question did this study set out to answer?

The study aims to explore whether nicotinamide riboside can reduce the harmful effects of antiphospholipid antibodies on trophoblast cells.

January 14, 2026

Nicotinamide Riboside Mitigates Antiphospholipid Antibody‐Induced Dysfunction in Human Trophoblast Cells

Key Points

The study aims to explore whether nicotinamide riboside can reduce the harmful effects of antiphospholipid antibodies on trophoblast cells.
Used human first-trimester trophoblast cell line Sw.71 for experimentation.
Trophoblasts were treated with antiphospholipid antibodies and nicotinamide riboside.
Cytokine and angiogenic factor levels were measured using ELISA.
Cell migration was assessed through a two-chamber colorimetric assay.
Reactive oxygen species (ROS) production was quantified using a fluorescence assay.
Nicotinamide riboside reduced inflammation and ROS production induced by antiphospholipid antibodies.
It restored angiogenic factor production affected by antiphospholipid antibodies.
Nicotinamide riboside did not improve the migratory dysfunction caused by antiphospholipid antibodies.

Abstract

ABSTRACT Problem Obstetric antiphospholipid syndrome (APS) is characterized by the presence of circulating anti‐phospholipid antibodies (aPL), which disrupt early placentation and contribute to adverse pregnancy outcomes including pregnancy loss and preterm birth. aPL, specifically those targeting beta 2 glycoprotein 1 (β 2 GPI), interact with placental trophoblast cells and induce inflammation, disrupt angiogenic factor production, and reduce cell migration. In addition, aPL have been shown to promote a state of oxidative stress in trophoblast cells and in APS patients. This study aimed to investigate if the antioxidant, nicotinamide riboside (NR), could mitigate the negative effects of aPL on trophoblast cells. Method of Study The human first‐trimester trophoblast cell line, Sw.71, was treated with or without aPL in the presence or absence of NR. Trophoblast supernatants were measured by ELISA for pro‐inflammatory cytokines/chemokines and angiogenic factors. Cell migration was measured using a two‐chamber colorimetric assay. ROS production was measured using a fluorescence assay. Results NR blocked aPL‐induced trophoblast inflammation and ROS production, and reversed the effects of aPL on trophoblast angiogenic factor production. However, NR was unable to rescue aPL‐induced trophoblast migratory dysfunction. Conclusion NR mitigated some, but not all, aPL‐induced trophoblast dysfunction. This provides new insight into the role of antioxidant therapies on aPL‐induced pregnancy complications, and a possible new avenue of managing obstetric APS to explore further.

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