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[Protective effects of astilbin on renal ischemia-reperfusion injury in rats]. | LitMetric

[Protective effects of astilbin on renal ischemia-reperfusion injury in rats].

Zhong Xi Yi Jie He Xue Bao

Organ Transplantation Center, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.

Published: August 2009

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.

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Source
http://dx.doi.org/10.3736/jcim20090809DOI Listing

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