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.
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