These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Delphinidin protects β2m-/Thy1+ bone marrow-derived hepatocyte stem cells against TGF-β1-induced oxidative stress and apoptosis through the PI3K/Akt pathway in vitro.
    Author: Chen J, Li HY, Wang D, Guo XZ.
    Journal: Chem Biol Interact; 2019 Jan 05; 297():109-118. PubMed ID: 30365941.
    Abstract:
    β2m-/Thy1+ bone marrow-derived hepatocyte stem cells (BDHSCs) have a potential to be applied for cellular treatment in liver cirrhosis. However, the resultant tissue regeneration is restricted by transplanted cells' death. The accumulation of transforming growth factor beta 1 (TGF-β1) in liver fibrosis local microenvironment may play an essential role in the rapid cell death of implanted β2m-/Thy1+ BDHSCs. The main mechanism of poor survival of the target stem cells is still unknown. Delphinidin, an anthocyanidin, has potent antioxidant and anti-inflammatory activities. However, whether this bio-active ingredient can substantially contribute to β2m-/Thy1+ BDHSCs' protection from TGF-β1 induced apoptosis in vitro remains to be elucidated. In the present research, we determined whether delphinidin pretreatment can improve the survival of β2m-/Thy1+ BDHSCs during exposure to TGF-β1 and elucidated its underlying mechanisms. By using TGF-β1, we induced the apoptosis of β2m-/Thy1+ BDHSCs and assessed the apoptotic rates up to 24 h by flow cytometry. β2m-/Thy1+ BDHSC proliferation was gauged using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl- 2H-tetrazolium bromide (MTT) assay. The expression grades of Bcl-2, Akt, caspase-3, and Bax were observed through Western blot analysis. We found that delphinidin can significantly impede TGF-β1-induced apoptosis dose-dependently, scavenge reactive oxygen species (ROS), and inhibit the discharge of caspase-3 in β2m-/Thy1+ BDHSCs. We also demonstrated that delphinidin can activate the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway. The suppression of ROS and succeeding apoptosis was achieved by pretreatment with LY294002, a PI3K/Akt pathway inhibitor. In summary, our findings revealed that delphinidin can protect β2m-/Thy1+ BDHSCs from apoptosis and ROS-dependent oxidative stress induced by the TGF-β1 via PI3K/Akt signaling pathway. On the basis of these data, delphinidin can be regarded as a promising anti-apoptotic agent for enhancing β2m-/Thy1+ BDHSC survival during cell transplantation in liver cirrhosis patients.
    [Abstract] [Full Text] [Related] [New Search]