Adipose-derived mesenchymal stem cells therapy for acute kidney injury induced by ischemia-reperfusion in a rat model.
Jian-Bo ZhangXiao-Qiao WangGuo-Lin LuHuan-Sen HuangShi-Yuan XuPublished in: Clinical and experimental pharmacology & physiology (2017)
Acute kidney injury (AKI) represents a group of complicated syndromes with a high mortality rate. The administration of adipose-derived mesenchymal stem cells (ADMSCs) has been tested as a possible treatment method for AKI. The long-term evaluation of AKI induced by ischemia/reperfusion (IR) and the probable renal protection of ADMSCs are limited. In this study we have established a rat AKI model induced by IR and investigated the possible protective effects of ADMSCs. Adult Sprague-Dawley (SD) rats were divided into three groups (n = 6/each group). The MOCK group was as the normal control. Rats in the IR-AKI and IR-AKI+ADMSCs groups were subjected to IR injury by clamping both renal pedicles for 40 minutes. Rats in the MOCK and IR-AKI groups were injected with PBS via the tail vein as negative treatment controls. Rats in the IR-AKI+ADMSCs group received ADMSCs therapy (2 × 106 cells were injected into the rats via the tail vein). We found that ADMSC transplantation restored the pathologic morphology induced by IR-AKI to normal compared with the MOCK group, suggesting the reparative function of ADMSCs in kidney tissues. Compared with IR-induced AKI alone, ADMSC treatment significantly decreased the number of apoptotic cells, the level of total urinary protein and serum creatinine, the expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β, IFN-γ, TNF-α, IFN-γ, and TGF-β), and the inflammation-associated proteins (HGF and SDF1), but increased the expression of the anti-inflammatory cytokine, IL-10, and the anti-apoptotic regulator, Bcl-2. Our data have indicated that ADMSC transplantation may protect against IR-induced AKI by anti-apoptotic and anti-inflammatory effects.
Keyphrases
- acute kidney injury
- cardiac surgery
- anti inflammatory
- mesenchymal stem cells
- cell death
- induced apoptosis
- oxidative stress
- rheumatoid arthritis
- immune response
- poor prognosis
- gene expression
- radiation therapy
- cardiovascular disease
- cell cycle arrest
- diabetic rats
- cardiovascular events
- adipose tissue
- binding protein
- small molecule
- transcription factor
- dendritic cells
- stem cells
- endothelial cells
- signaling pathway
- epithelial mesenchymal transition
- insulin resistance
- mass spectrometry
- replacement therapy
- drug induced