AI Article Synopsis
- The study explored the effects of aminoguanidine (AG) on nerve damage related to sciatic nerve ischemia-reperfusion injury in rats.
- Treatment with AG significantly improved the sciatic functional index (SFI) and reduced malondialdehyde (MDA) levels during the 7th and 14th days of recovery.
- AG appears to help mitigate oxidative stress and apoptosis, indicating its potential as a protective treatment for nerve injuries caused by blood flow disruption.
Article Abstract
This study was conducted to investigate the potential protective effects of aminoguanidine (AG) on sciatic functional index (SFI), oxidative stress status, and apoptosis index using a rat model of experimental sciatic nerve ischemia-reperfusion injury (I/R). Treatment groups received 150 mg AG/kg body mass, 24 h after the induction of ischemia. After reperfusion for 2, 4, 7, 14, and 28 days, we evaluated measured SFI, plasma antioxidant enzymes, total antioxidant capacity (TAC), malondialdehyde (MDA), and index of apoptosis. SFI was significantly improved on the 7th and 14th day of reperfusion in the AG-treated groups. AG treatment resulted in the significant reduction of MDA levels on the 7th and 14th day of reperfusion. TAC was only increased after 7 days of reperfusion compared with the untreated group. SOD activity was decreased in both the untreated and AG-treated groups by comparison with the control, but did not show a significant change. GPx activity decreased only after 7 days of reperfusion. The maximal rate of apoptosis occurred on the 7th day of reperfusion. Treatment with AG significantly reduced this enhancement. AG exhibits positive effects against sciatic nerve I/R injury, possibly in part because of the protective effects of AG against apoptosis and I/R-induced oxidative stress.
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| http://dx.doi.org/10.1139/cjpp-2014-0315 | DOI Listing |
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