Effect of combination of vitamin E and umbilical cord-derived mesenchymal stem cells on inflammation in mice with acute kidney injury.

BACKGROUND

The objective of this study is to investigate the effect of combination of umbilical cord-derived mesenchymal stem cell (UC-MSC) and vitamin E (VitE) on inflammation in mice with acute kidney injury (AKI).

METHODS

UC-MSCs were isolated from pregnant wistar mice and cultured. A total of 90 female wistar mice were randomly divided into control group, AKI group, AKI + VitE group, AKI + UC-MSC group, and AKI + VitE + UC-MSC group (18 mice in each group) which were given no treatment, normal saline, VitE, UC-MSC, and VitE + UC-MSC, respectively. The renal pedicles on both sides were clipped for 50 min with micro-artery clips to induce AKI. Six mice were sacrificed at days 1, 3, and 7, while blood and kidney tissues were collected to detect levels of blood urea nitrogen (BUN) and creatinine (Scr). Kidney tissues were stained by HE staining to observe pathological changes; levels of interleukin-lβ, TNF-α, interleukin-10, and β-FGF were measured by ELISA.

RESULTS

Compared with the control group, AKI mice showed higher levels of serum BUN and Scr, tubular swelling and necrosis suggesting that AKI model was successfully established. Mice in AKI + VitE group, AKI + UC-MSC group, and AKI + VitE + UC-MSC presented better renal function than mice of AKI group. Mice from AKI + VitE + UC-MSC group showed the best renal function with the least renal tubular injury (p < .05). ELISA detection revealed that pro-inflammatory cytokines were significantly increased and anti-inflammatory cytokine levels were significantly decreased in all time points (p < .05). VitE, UC-MSC, and VitE + UC-MSC resulted in the increase of anti-inflammatory cytokine levels and reduction of pro-inflammatory cytokine levels and the combination of VitE and UC-MSC performed favorable effect in the suppression of inflammation in AKI mice (p < .05).

CONCLUSIONS

Combination of UC-MSC and VitE significantly inhibited inflammatory reaction in kidney through the regulation of inflammatory cytokines in the microenvironment of kidney with AKI. Combination of UC-MSC and VitE presented therapeutic effect on AKI than the single use of UC-MSC or VitE.