Investigation of the effects of umbilical cord and adipose-derived mesenchymal stem cells on endoplasmic reticulum stress in cadmium-induced rat kidney.

Purpose: The hazardous heavy metal cadmium (Cd) has the potential to cause long-term kidney damage, mostly dependent on autophagy. Endoplasmic reticulum (ER) stress has been recognized as a primary source of Cd-induced toxicity. The ER chaperone GRP78 binds ER stress sensors, keeping them dormant. Exposure to Cd increases ER stress, a well-known inducer of autophagy. Adipose-derived mesenchymal stem cells (AD-MSC) are potentially useful tissue engineering and cellular treatment tools. Various disorders are treated with human umbilical cord MSCs (HUC-MSCs). They possess several unique qualities that are necessary for their therapeutic uses. The study aimed to investigate the effects of AD-MSCs and HUC-MSCs on Cd-induced nephrotoxicity.

Methods: The study used 36 male Wistar albino rats that were divided into six groups: control, AD-MSC, HUC-MSC, Cd, Cd ​+ ​AD-MSC, and Cd ​+ ​HUC-MSC. Hematoxylin and eosin (H&E) were used to stain the renal tissues in preparation for a histological analysis. Furthermore, the ER stress level was assessed by measuring GRP78 immunoexpression. Additionally, LC3B and Beclin-1 immunostaining were used to determine the autophagy.

Results: The histopathological results showed that the glomerular structure, proximal and distal tubules were disrupted in rat kidneys from the Cd group. Treatment with AD-MSCs and HUC-MSCs restored renal histological damage caused by Cd. Additionally, in Cd-induced renal tissues, there was an increase in the immunoexpression of the autophagic sensors LC3B and Beclin-1 and the ER stress indicator GRP78.

Conclusion: MSCs enabled Cd-damaged kidney tissues to regain an almost healthy histological structure.