Introduction:
Acute kidney injury (AKI) is a diverse set of illnesses characterized by a rapid decline in kidney function

Material and methods:
Characteristics and homing of MSCs to kidney tissues were identified by flow cytometry and differentiation capability. After AKI induction by cisplatin injection in sixteen albino rats, the AKI rats were further subdivided into three subgroups. The first subgroup served as a positive control and the second one received 2 mg/kg furosemide (FUR) which served as a standard drug. The third subgroup received a single dose of 5 x 106 MSCs via tail vein injection once a week for consecutive two weeks. AKI-related biochemical parameters were assayed at 2 weeks after MSC treatment. Kidney histological changes were also evaluated. Moreover, the apoptosis of kidney cells and expression of apoptosis-related proteins were assessed by western blot.

Results:
Compared with AKI rats, rats treated with MSCs showed suppressed serum levels of creatinine and blood urea nitrogen. MSC treatment alleviated the pathological abnormalities in the kidneys of AKI rats as shown by H&E staining.Furthermore, MSC treatment suppressed apoptosis of kidney cells in AKI rats via downregulation of apoptotic proteins; thioredoxin-interacting protein (TXNIP) and apoptosis signal-regulating kinase 1 (ASK1). Most importantly, MSC treatment promoted the expression of vascular endothelial growth factor (VEGF) in the kidneys of AKI rats.

Conclusions:
Our results suggest that MSCs could ameliorate renal injury of AKI rats via their antiapoptotic properties. Also, the protective effects of MSCs may be mediated by their angiogenic potential effects.