Effects of butein on renal ischemia/reperfusion injury: An experimental study

Objectives: Renal ischemia/reperfusion (I/R) injury is a common cause of acute kidney injury. The aim of this study was to investigate the effect of butein on renal I/R injury. Materials and methods: Twenty-seven rats were randomly allocated to three groups (n = 9): a sham group, a renal I/Runtreated (control) group, and a renal I/R-butein group. The sham group underwent only opening and closing of the peritoneum. In the control group, an experimental I/R model was created and 1 cc isotonic saline was applied to the peritoneum. In the butein group, the experimental I/R model was created and 1 mg/kg butein was administered intraperitoneally 15 minutes before the beginning of ischemia. The left kidneys of the rats were histopathologically examined for tissue damage caused by I/R. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. By contrast, 2 in the control group (22.2%) had small focal damaged areas, 1 (11.1%) had < 10% cortical damage, 5 (55.6%) had 10-25% cortical damage, and 1 (11.1%) had 25-75% cortical damage. The butein group had 1 (11.1%) normal kidney, 2 (22.2%) with small focal damaged areas, 4 (44.4%) with < 10% cortical damage, and 2 (22.2%) with 10-25% cortical damage. Tissue damage was significantly lower in the sham group than in the control and butein groups (p < 0.01). No statistically significant differences were observed in the histopathology of the control and butein groups (p > 0.05). Conclusions: Intraperitoneal administration of butein had no significant effect on renal tissue injury.

Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

Organophosphorus insecticides including chlorpyrifos (CPF) are mainly used for agriculture, household, and military purposes; their application is associated with various adverse reactions in animals and humans. This study was conducted to evaluate the potential neuroprotective effect of red beetroot methanolic extract (RBR) against CPF-induced cortical damage. Twenty-eight adult male Wistar albino rats were divided into 4 groups (n=7 in each group): the control group was administered physiological saline (0.9% NaCl), the CPF group was administered CPF (10 mg/kg), the RBR group was administered RBR (300 mg/kg), and the RBR+CPF group was treated with RBR (300 mg/kg) 1 hr before CPF (10 mg/kg) supplementation. All groups were treated for 28 days. Rats exposed to CPF exhibited a significant decrease in cortical acetylcholinesterase activity and brain-derived neurotrophic factor and a decrease in glial fibrillary acidic protein. CPF intoxication increased lipid peroxidation, inducible nitric oxide synthase expression, and nitric oxide production. This was accompanied by a decrease in glutathione content and in the activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase in the cortical tissue. Additionally, CPF enhanced inflammatory response, indicated by increased levels and expression of interleukin-1β and tumor necrosis factor-α. CPF triggered neuronal apoptosis by upregulating Bax and caspase-3 and downregulating Bcl-2. However, RBR reversed the induced neuronal alterations following CPF intoxication. Our findings suggest that RBR can minimize and prevent CPF neurotoxicity through its antioxidant, anti-inflammatory, and antiapoptotic activities.