Brassicaceae are rich in healthy phytochemicals that have a positive impact on human health. The aim of this study was to analyze the phenolic compounds and antioxidant and anticancer potential of traditional Croatian kale (Brassica oleracea L. var. acephala DC.) and wild cabbage (Brassica incana Ten.) extracts. The phenolic groups and antioxidant activity were determined by spectrophotometry, selected phenolic compounds (ferulic acid, sinapic acid, salicylic acid, kaempferol, and quercetin) were analyzed by LC-MS/MS, and anticancer potential was evaluated in vitro using HeLa cells. The extracts of both plant species are rich in phenolic compounds and showed significant antioxidant activity at similar levels. LC-MS/MS detected sinapic acid as the most abundant phenolic acid, followed by ferulic acid, while salicylic acid was present at lower concentrations. A comparative analysis showed that wild cabbage contained significantly more sinapic acid, while kale contained more kaempferol and quercetin. Both Brassica extracts at a concentration of 50 µg mL⁻¹ showed an antiproliferative effect on HeLa cells, while they did not affect the proliferation of normal human skin fibroblasts. Wild cabbage extract also showed an antiproliferative effect on HeLa cells at a lower applied concentration of 10 µg mL⁻¹ of extracts. The clonogenic analysis also revealed the inhibitory effect of the extracts on HeLa colony growth.

Alzheimer's disease (AD) is the most common neurodegenerative disorder associated with insulin resistance and glucose hypometabolism in the brain. Oral administration of galactose, a nutrient that provides an alternative source of energy, prevents and ameliorates early cognitive impairment in a streptozotocin-induced model (STZ-icv) of the sporadic AD (sAD). Here we explored the influence of 2-month oral galactose treatment (200 mg/kg/day) in the familial AD (fAD) by using 5- (5M) and 10- (10M) month-old transgenic Tg2576 mice mimicking the presymptomatic and the mild stage of fAD, and compared it to that observed in 7-month old STZ-icv rats mimicking mild-to-moderate sAD. Cognitive and behavioral performance was tested by Morris Water Maze, Open Field and Elevated Plus Maze tests, and metabolic status by intraperitoneal glucose tolerance test and fluorodeoxyglucose Positron-Emission Tomography scan. The level of insulin, glucagon-like peptide-1 (GLP-1) and soluble amyloid β1-42 (sAβ1-42) was measured by ELISA and the protein expression of insulin receptor (IR), glycogen synthase kinase-3β (GSK-3β), and pre-/post-synaptic markers by Western blot analysis. Although galactose normalized alterations in cerebral glucose metabolism in all Tg2576 mice (5M+2M; 10M+2M) and STZ-icv rats, it did not improve cognitive impairment in either model. Improvement of reduced grooming behavior and normalization in reduced plasma insulin levels were seen only in 5M+2M Tg2576 mice while in 10M+2M Tg2576 mice oral galactose induced metabolic exacerbation at the level of plasma insulin, GLP-1 homeostasis and glucose intolerance, and additionally increased hippocampal sAβ1-42 level, decreased IR expression and increased GSK-3β activity. The results indicate that therapeutic potential of oral galactose seems to depend on the stage and the type/model of AD and to differ in the absence and the presence of AD-like pathology.

The relationship between hemochromatosis and diabetes has been well established, as excessive iron deposition has been reported to result in impaired function of the endocrine and exocrine pancreas. Therefore, the objective of the present study was to analyze the effects of iron accumulation on the pancreata and glucose homeostasis in a bone morphogenetic protein 6‑knockout (Bmp6^‑/‑) mouse model of hemochromatosis. The sera and pancreatic tissues of wild‑type (WT) and Bmp6^‑/‑ mice (age, 3 and 10 months) were subjected to biochemical and histological analyses. In addition, ¹⁸F‑fluorodeoxyglucose biodistribution was evaluated in the liver, muscle, heart, kidney and adipose tissue of both animal groups. The results demonstrated that 3‑month‑old Bmp6^‑/‑ mice exhibited iron accumulation preferentially in the exocrine pancreas, with no signs of pancreatic injury or fibrosis. No changes were observed in the glucose metabolism, as pancreatic islet diameter, insulin and glucagon secretion, blood glucose levels and glucose uptake in the liver, muscle and adipose tissue remained comparable with those in the WT mice. Aging Bmp6^‑/‑ mice presented with progressive iron deposits in the exocrine pancreas, leading to pancreatic degeneration and injury that was characterized by acinar atrophy, fibrosis and the infiltration of inflammatory cells. However, the aging mice exhibited unaltered blood glucose levels and islet structure, normal insulin secretion and moderately increased α‑cell mass compared with those in the age‑matched WT mice. Additionally, iron overload and pancreatic damage were not observed in the aging WT mice. These results supported a pathogenic role of iron overload in aging Bmp6^‑/‑ mice leading to iron‑induced exocrine pancreatic deficiency, whereas the endocrine pancreas retained normal function.