Regulatory effect of immunosuppressive agents in mice with renal ischemia reperfusion injury
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- Published online on: August 22, 2018 https://doi.org/10.3892/etm.2018.6642
- Pages: 3584-3588
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Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
This study was designed to investigate the regulatory effect of rapamycin in mice with renal ischemia‑reperfusion injury. A total of 100 mice were randomly divided into normal control, sham operation, model and experimental groups with 25 rats in each group. Mice in the experimental group were subjected to rapamycin gavage. Mice in each group were sacrificed 24 h after operation. Then, blood, spleen and left kidney were collected. PAS staining was used for semi‑quantitative analysis of renal pathological injury. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were measured. TUNEL method was used to detect cell apoptosis. Flow cytometry was used to detect the percentage of NKT cells. The expression of CXC chemokine ligand 10 (CXCL10), hypoxia‑inducible factor‑1α (HIF‑1α) and vascular endothelial growth factor (VEGF) mRNA were detected by RT‑qPCR. Semi‑quantitative scoring of renal pathological injury showed that pathological injury score of the experimental group was significantly lower than that of the model group (p<0.05). Serum levels of SCr and BUN in the experimental group was compared to those in the model group (p<0.05). The number of apoptotic cells in the experimental group was compared to that of the model group (p<0.05). The percentage of NKT cells in the experimental group was compared to that of the model group (p<0.05). The percentage of NKT cells was significantly higher in the kidney and peripheral blood of the experimental group than that in the model group (p<0.05). The expression levels of HIF‑1α and VEGF mRNA in the model and experimental groups were significantly lower in the experimental group than those in the model group (p<0.05). The expression levels of CXCL10 mRNA in the model and experimental groups were significantly higher in the experimental group than those in the model group (p<0.05). The results indicated that rapamycin can significantly upregulate the expression level of CXCL9 and promote the accumulation of NKT cells in kidney from spleen through peripheral blood. Rapamycin can also inhibit the HIF‑1α expression level and protect renal ischemia‑reperfusion injury.
