Tauroursodeoxycholic Acid Inhibited Apoptosis and Oxidative Stress in ­H2O2‑Induced BMSC Death via Modulating the Nrf‑2 Signaling Pathway: the Therapeutic Implications in a Rat Model of Spinal Cord Injury

Spinal cord injury (SCI) often results in motor and sensory dysfunction, and current solutions are lacking. Bone marrow mesenchymal stem cells (BMSCs) have emerged as a potential treatment, but their effectiveness is limited by low survival and differentiation rates due to the oxidative stress (OS) microenvironment. Tauroursodeoxycholic acid (TUDCA), found in bear bile, has shown neuroprotective effects. This study investigates whether combining TUDCA with BMSC transplantation enhances therapeutic benefits in SCI. The study found that TUDCA significantly enhanced BMSC viability, reduced apoptosis and oxidative stress both in vitro and in vivo, and accelerated tissue regeneration and functional recovery following BMSC transplantation in SCI rats, potentially by activating the Nrf-2 signaling pathway.

• 1
  TUDCA significantly enhanced BMSC viability and reduced apoptosis (assessed by Annexin V-FITC, TUNEL, Bax, Bcl-2, and Caspase-3) as well as oxidative stress (assessed by ROS, GSH, SOD, and MDA) both in vitro and in vivo.
• 2
  TUDCA accelerated tissue regeneration (assessed by HE, Nissl, MAP2, MBP, TUJ1, and GFAP) and improved functional recovery (assessed by BBB score) following BMSC transplantation in SCI.
• 3
  These effects were mediated via the Nrf-2 signaling pathway, as evidenced by the upregulation of Nrf-2, NQO-1, and HO-1 expression levels.