3. MATERIALS AND METHODS
hucMSCs isolation and identification
CM-Dil cell-labelling
Cell co-culture
Cisplatin-induced renal injury rat model (6.0 mg/kg)
hucMSCs transplantation (intraperitoneally injection)
Renal function and Malondialdehyde (MDA) determination
Histopathology and Masson’s trichrome staining
TUNEL staining and immunohistochemistry
Quantitative RT-PCR
Western blot
5. hucMSCs promote proliferation of and inhibit
apoptosis and alleviate inflammation in cisplatin-induced
AKI rats in the renal tubular cells of cisplatin-induced
AKI rats
6. hucMSCs protect renal cell mitochondria from
dysfunction and inhibit the activation of mitochondrial
apoptosis signaling
10. Conclusion
In conclusion,results demonstrate that hucMSCs attenuate cisplatin-induced acute
and chronic renal injury through preventing mitochondria dysfunction, inhibiting
the activation of mitochondrial signaling pathway and suppressing the
development of EMT.
These findings suggest that hucMSC transplantation is a useful approach for the
therapy of cisplatin-induced AKI and the subsequent renal interstitial fibrosis.