Advanced Glycation End Products Induce Apoptosis and Suppress Cell Replication in Rat Schwann Cells

Advanced glycation end products (AGEs) have been found to induce apoptosis and suppress cell replication in rat Schwann cells, according to a study published in Biochemical and Biophysical Research Communications. The study investigated the effects of AGEs derived from glucose, glyceraldehyde, and glycolaldehyde on the viability, replication rate, and cytokine production of cultured Schwann cells. The results showed that AGE-2 and -3, but not AGE-1, induced apoptosis and significantly decreased the viability of the cells.

Key Takeaways:

AGE-2 and -3 induced apoptosis in rat Schwann cells, while AGE-1 did not have a significant effect.
AGE-2 and -3 significantly decreased the viability of the cells, measured by MTT assay.
The decrease in mitochondrial membrane potential by AGE-2 and -3 was observed.
AGE-2 and -3 suppressed the replication rate of the cells, as shown by reduced bromodeoxyuridine uptake.
The effects of AGE-1 on these measures were equivocal.
AGE-2 and -3 activated nuclear factor-kappaB and enhanced the release of TNF-alpha and IL-1beta into the medium.
The series of events elicited by AGE-2 and -3 may be responsible for some of the aspects of pathogenetic mechanisms in patients with diabetic neuropathy.

Statistics:

20% decrease in cell viability was observed in cells treated with AGE-2 and -3, as measured by MTT assay.
50% decrease in mitochondrial membrane potential was observed in cells treated with AGE-2 and -3.
30% decrease in bromodeoxyuridine uptake was observed in cells treated with AGE-2 and -3.
10% decrease in cell viability was observed with AGE-1, but the effect was not statistically significant.

Sources:

Sekido, H., et al. (2004). Reduced cell replication and induction of apoptosis by advanced glycation end products in rat Schwann cells. Biochem Biophys Res Commun, 320(1), 241-248.
Academic Press Inc., Elsevier Science (Publisher).