Intra-tracheal delivery of mesenchymal stem cell-conditioned medium ameliorates pathological changes by inhibiting apoptosis in asthmatic rats

Mol Biol Rep. 2022 May;49(5):3721-3728. doi: 10.1007/s11033-022-07212-8. Epub 2022 Feb 3.

Abstract

Background: Asthma, an inflammatory illness of the lungs, remains the most common long-term disease amongst children. This study tried to elaborate the status of apoptosis in asthmatic pulmonary niche after the application of rat mesenchymal stem cells (MSC-CM)-derived secretome.

Methods and results: Here, we randomly allocated male Wistar rats into three groups (n = 8); Control animals were intratracheally given 50 μl vehicle. In control-matched sensitized rats, 50 μl normal saline was used. In the last group, 50 μl MSC-CM was applied. Two-week post-administration, transcription of T-bet, GATA-3, Bax, Bcl-2 and Caspase-3 was measured by gene expression analysis. Pathological injuries were monitored using H&E staining. The BALF level of TNF-α was measured using ELISA assay. In asthmatic rats received MSC-CM, the expression of T-bet was increased while the level of GATA-3 decreased compared to the S group (p < 0.05). Levels of BALF TNF-α were suppressed in asthmatic niche after MSC-CM administration (p < 0.05). Compared to the asthmatic group, MSC-CM had potential to alter the expression of apoptosis-related genes in which the expression of Bax and Caspase 3 was decreased and the expression of pro-survival factor, Bcl-2 increased (p < 0.05).

Conclusion: Our data notified the potency of direct administration of MSC-CM in the alleviation of airway inflammation, presumably by down regulating apoptotic death in pulmonary niche.

Keywords: Apoptosis; Asthma; Condition medium; Mesenchymal stem cells; Rats.

MeSH terms

  • Animals
  • Apoptosis
  • Asthma* / metabolism
  • Culture Media, Conditioned / pharmacology
  • Lung / metabolism
  • Male
  • Mesenchymal Stem Cells* / metabolism
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • bcl-2-Associated X Protein / genetics
  • bcl-2-Associated X Protein / metabolism

Substances

  • Culture Media, Conditioned
  • Tumor Necrosis Factor-alpha
  • bcl-2-Associated X Protein