Supported with significant rejuvenating and regenerating actions of mesenchymal stem cells (MSCs) in various
gastrointestinal diseases including Helicobacter pylori (H. pylori)-associated
gastric diseases, we have compared these actions among placenta derived-MSCs (PD-MSCs), umbilical cord derived-MSCs (UC-MSCs), and adipose tissue derived-MSCs (AD-MSCs) and explored contributing genes implicated in
rejuvenation of H. pylori-chronic
atrophic gastritis (CAG) and
tumorigenesis. In this study adopting H. pylori-initiated, high
salt diet-promoted gastric
carcinogenesis model, we have administered three kinds of MSCs around 15-18 weeks in H. pylori infected C57BL/6 mice and sacrificed at 24 and 48 weeks, respectively, in order to either assess the rejuvenating capability or anti-
tumorigenesis. At 24 weeks, MSCs all led to significantly mitigated
atrophic gastritis, for which significant inductions of autophagy, preservation of
tumor suppressive
15-PGDH, attenuated apoptosis, and efficient efferocytosis was imposed with MSCs administration during
atrophic gastritis. At 48 weeks, MSCs administered during H. pylori-associated
atrophic gastritis afforded significant blocking the progression of CAG, as evidenced with statistically significant reduction in H. pylori-associated gastric
tumor (p<0.05) accompanied with significant decreases in IL-1β, COX-2, STAT3, and NF-κB. Combined together with the changes of stanniocalcin-1 (STC-1), thrombospondin-1 (TSP-1), and
IL-10 known as
biomarkers reflecting stem cell activities at 48 weeks after H. pylori, PD-MSCs among MSCs afforded the best rejuvenating action against H. pylori-associated CAG via additional actions of efferocytosis, autophagy, and anti-apoptosis at 24 weeks. In conclusion, MSCs, especially PD-MSCs, exerted rejuvenating actions against H. pylori-associated CAG via anti-mutagenesis of
IL-10, CD-36, ATG5 and
cancer suppressive influences of STC-1,
TSP-1, and
15-PGDH.