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Updated: Jun 21, 2026

Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
Published on: November 3, 2023
[Protective effects of astilbin on renal ischemia-reperfusion injury in rats]
Shao-Hua Song1, Xiao-Yun Shen, Fang Liu
1Organ Transplantation Center, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Objective:
To investigate the protective effects of astilbin on renal ischemia-reperfusion (IR) injury in rats.
Methods:
Twenty-four male SD rats, two months old, were randomly allocated into three groups: sham-operated group (n=8), untreated group (n=8) and astilbin group (n=8). Rats in the untreated group and the astilbin group underwent temporary renal artery occlusion to induce IR injury. The rats in the astilbin group were intraperitoneally injected with 12 mg/mL astilbin at a dose of 30 mg/kg from 3 day before IR injury until to be sacrificed once per day, and rats in the untreated group were injected with equal volume of normal saline at the same time. After 6-hour reperfusion, blood urea nitrogen (BUN) and serum creatinine (SCr) and histological changes of the renal tissues were detected to evaluate renal injury. Expressions of monocyte chemoattractant protein-1 (MCP-1) mRNA and protein in the renal tissues and the serum contents of interleukin-6 (IL-6) and IL-1beta were also measured with semi-quantitative reverse transcription-polymerase chain reaction, Western blotting or enzyme-linked immunosorbent assay.
Results:
Compared with the untreated group, BUN and SCr levels were significantly decreased in the astilbin group after 6-hour reperfusion (P<0.01), and similar results were also found in histological examination. The expressions of MCP-1 mRNA and protein in renal tissues in the astilbin group were lower than those in the untreated group. The serum contents of IL-6 and IL-1beta were decreased in the astilbin group as compared with the untreated group (P<0.01).
Conclusion:
Astilbin can ameliorate kidney IR injury in rats by inhibiting the production of chemokine MCP-1 and cytokines IL-6 and IL-1beta.

