ABSTRACT
OBJECTIVE: Hyperglycaemia is an important risk factor for the development and progression of the macrovascular and microvascular complications that occur in diabetes. The expression of apoptotic markers in the aortic medial layer of diabetic rats and the effects of N. sativa L. seed oil on the expression of these markers were investigated in this study. METHODS: Four-month-old adult female Wistar rats (n=21) were divided into 3 groups: Group 1, control; Group 2, diabetes and Group 3, diabetes+N. sativa L. seed oil. Group 3 received 0.2 mg/kg/day N. sativa L. seed (black cumin) oil intraperitoneally 6 days per week for 30 days. At the end of the experiment, abdominal and thoracic aortas of all animals were collected and fixed in 10% formalin solution. Then, 5-µm-thick sections were stained with Verhoeff-Van Gieson stain to evaluate Bax and Caspase 3 expression. Tunica intima-media thickness was measured using the stained sections. RESULTS: There were no significant differences in abdominal or thoracic aortic intima-media thickness among the 3 groups. However, there were significant differences in Bax and Caspase 3 expression in the tunica media of the thoracic and abdominal aortas between Group 1 and Group 2 (p<0.05) and between Group 2 and Group 3 (p<0.05) evaluated with the Kruskal-Wallis and Mann-Whitney U tests. CONCLUSION: It is understood that N. sativa L. seed oil is effective against diabetes. N. sativa L. seed oil is a plant material and has value for further investigation to develop diabetes treatment strategies for preventing apoptosis in vascular structures.
ABSTRACT
Cyclophosphamide (CP) has a range of adverse effects on liver tissue in humans and animals. Administering an antioxidant with CP might reduce such side effects. Therefore, we examined the role of vitamin E in CP-induced liver toxicity in rats. Male Wistar albino rats were divided into four groups, each of seven rats: control, CP only, CP + vitamin E, and vitamin E only groups. The rats were administered treatments intraperitoneally for 7 days. Then the serum malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate transaminase (AST), and lactate dehydrogenase (LDH) levels were determined while the livers were removed, tissue was prepared using routine histological procedures, sections were stained using hematoxylin and eosin, and the terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) method was applied. Histopathologically, CP caused hydropic degeneration, necrosis, pleomorphism, and mitotic activity. The number of TUNEL-positive cells and the MDA and ALT levels were significantly higher in the CP group. The antioxidant effects of vitamin E significantly decreased the number of TUNEL-positive cells and the ALT and MDA levels, and normalized the liver histopathology. CP induces apoptosis, has toxic effects on liver tissue, and changes the histological structure. The administration of vitamin E prevented the liver tissue damage caused by CP.
