Acacetin Alleviates Hepatitis Following Renal Ischemia-Reperfusion in Male Balb/C Mice by Antioxidants Regulation and Inflammatory Markers Suppression.

BACKGROUND: Ischemia-reperfusion (Isc/Rep) incidence can damage kidneys and long-distance organs such as the liver. Due to the increasing use of herbs in medicine, this study was designed to assess the effects of Acacetin (ACA) on pathophysiology of liver following renal Isc/Rep induction. Methods: 84 male Balb/C mice were divided into 12 groups including control, control + ACAs groups (0.01% DMSO or 50, 25, 10 mg/kg of ACA.) sham group (a period of 60 min laparotomy with 0.01% DMSO treatment) sham + ACAs groups (0.01% DMSO + 50, 25, 10 mg/kg of ACA) Isc/Rep treatment groups (laparotomy and bilateralrenal occlusion for 60 min with/without administration of 50, 25, 10 mg/kg ACA). All experimental groups were treated intraperitoneally daily for 4 consecutive days. The values of quantitative histology, Total Antioxidant Capacity (TAC), Nitric oxide (NO), TNFα, IL1ß, and the serum levels of hepatic enzymes were evaluated. Results: In the Isc/Rep and Isc/Rep + ACA (10 mg/kg) groups, there were a significant decrease in the level of albumin and TAC, while the other evaluated parameters were significantly increased (p < 0.05). In the Isc/Rep + ACA (25, 50 mg/kg), these parameters showed significant recovery compared to Isc/Rep + ACA (10 mg/kg) group (p < 0.05). Conclusion: Increasing the oxidant activity is the most important cause of injury in long-distance organs following Isc/Rep process. By employing the inflammatory mediators in a dose-dependent manner, the ACA reveals the recovery effects on liver failure.

Acacetin Attenuates Renal Damage-Induced by Ischemia-Reperfusion with Declining Apoptosis and Oxidative Stress in Mice.

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.