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ORIGINAL ARTICLE
Year : 2020  |  Volume : 11  |  Issue : 1  |  Page : 22

Acacetin attenuates renal damage-induced by ischemia-reperfusion with declining apoptosis and oxidative stress in mice


1 Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
2 Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran

Correspondence Address:
Alvand Alvani
Department of Biology, Damghan Branch, Islamic Azad University, Damghan
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpvm.IJPVM_512_18

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Background: Renal ischemia-reperfusion disturbs both the function and the histology of this organ. Acacetin (Aca) is a natural flavonoid that is effective for relief of many diseases. The aim of this study was to determine the impacts of Aca on renal ischemia-reperfusion process in mice. Methods: In total, 84 male Balb/cmice divided into 12 groups and were administrated intraperitoneally for 4 days with or without surgery to dimethyl sulfoxide 0.01% or Aca (10, 25, and 50 mg/kg) as Control, control Acas, sham, sham Acas groups. Ischemia-reperfusion without or with Aca (10, 25, and 50 mg/kg) treatments were the other groups. Parameters related to the function and the histology of the kidneys were evaluated and statistically analyzed from kidney and blood serum samples in the respect of the groups. Results: In ischemia-reperfusion and ischemia-reperfusion + Aca (10 mg/kg) groups, there were significantly increased in urea, creatinine, malondialdehyde (MDA), and apoptosis rate, whereas total antioxidant capacity decreased compared to the control and sham and ischemia-reperfusion + Aca (25 and 50 mg/kg) (P < 0.05). The histopathology alteration was seen in the ischemia-reperfusion group than the others (P < 0.01). Moreover, there was a significant difference between ischemia-reperfusion + Aca (25 and50 mg/kg) groups than ischemia-reperfusion + Aca (10 mg/kg) one (P < 0.05). Conclusions: The recovery effect of Aca was offered on renal ischemia-reperfusion damage in a dose-dependent manner in mice, showing by kidney histopathology and functional criteria improvements. The attributed mechanism for this impression would be the antioxidant property of Aca, decreasing both MDA levels and apoptosis rate in kidney tissue.


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