No abstract

We investigated possible effects of proanthocyanidin (PA) and vitamin E on damage to rat kidneys induced by formaldehyde (FA), using biochemical characteristics and light and electron microscopy. Male rats were divided into control, FA, PA and vitamin E treated groups. Kidney tissue was observed by light and electron microscopy. Bcl-2/Bax rate was measured using immunohistochemistry. Malondialdehyde (MDA) and total sialic acid (TSA) levels, superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase (CAT) and myeloperoxidase (MPO) activities were measured. We found that FA caused damage to the parietal epithelial layer of the glomerulus, mononuclear cell infiltration, membrane damage in renal tubules, pyknotic nuclei, hypertrophic cells in Henle's loop and tubules, and loss of renal tubule integrity. We also observed invagination of the nuclear membrane, irregularity of chromatin material and loss of mitochondrial cristae. We observed increased Bcl-2 and Bax immunostaining in the FA group, but the Bcl-2/Bax rate remained unchanged in FA, PA and vitamin E groups compared to controls. Tissue MDA and TSA levels, and CAT and Gpx activities were increased, and SOD and MPO activities were decreased by FA toxicity. We observed a protective effect of PA in tissue MDA and TSA levels and SOD activities, because there was no difference in the PA group compared to the control group. We investigated the antioxidant effects of PA and vitamin E and found protective effects of PA against apoptosis.

Background. Endometriosis is one of the most common chronic gynecological diseases. Objectives. The aim of the study was to examine the effects of curcumin and/or deferoxamine on cell proliferation in a rat model of endometriosis. Material and methods. Thirty female 12-week-old albino Wistar rats, weighing 200-250 g, were used in this study. All the rats underwent ovariectomy and 0.1-mg β-estradiol 17-valerate pellets were placed intraperitoneally. An experimental model of endometriosis was created in all the animals. To create the experimental model, an approximately 1-cm long section of the uterus was taken, primarily from the right horn of the uterus. Autologous fragments were then placed between the peritoneum and muscle. The animals were divided into 3 groups: Group A, treated only with the vehicle used for curcumin and deferoxamine; group B, treated with curcumin (100 mg/kg body weight); and group C, treated with deferoxamine + curcumin (100 mg/kg body weight). After biopsy samples were obtained, the sections were stained with hematoxylin and eosin. Immunostaining for cytokeratin-7 and proliferating cell nuclear antigen (PCNA) was performed. Blood iron levels were measured using a Perkin Elmer AAnalyst 800 Atomic Absorption Spectrophotometer. Results. The endometrial implant size increased in Group A, but treatment with curcumin (p = 0.01) and deferoxamine + curcumin (p = 0.007) reduced the implant size. In ectopic endometrial epithelial cells, there were significant decreases in PCNA immunoreactivity between groups A and B (p = 0.044) and between groups A and C (p = 0.033). Conclusions. Treatment with curcumin alone and/or in combination with deferoxamine contributed to a reduction in implant size and cell proliferation in a rat endometriosis model. Iron-chelating agents may act in the same manner when used in women with endometriosis; however, further studies from different perspectives are still needed.

We aimed to investigate of protective role of proanthocyanidin (PA) and vitamin E (vit E) against to toxic effect of formaldehyde (FA). Twenty-eight Wistar albino rats were divided into four groups: control group, rats treated with FA intraperitoneal (i.p.) (10 mg/kg), FA + vit E intragastric (i.g.) (30 mg/kg), and FA + PA i.g. (100 mg/kg). We assayed superoxide dismutase (SOD), glutathione peroxidase (Gpx), myeloperoxidase (MPO) activity and levels of malondialdehyde (MDA) and total sialic acid (TSA) in liver. Liver tissue was taken in order to morphological analysis and hepatocytes apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay immunostaining. SOD decreased in FA and increased in FA + vit E and FA + PA (p < 0.05). Gpx didn't change in FA and increased in FA + PA (p < 0.05). No significant variation between the groups was found in MPO activity. MDA increased only in FA and decreased in FA + vit E and FA+PA (p < 0.05). TSA didn't alter in FA and FA + vit E but decreased in FA + PA (p < 0.05). Degeneration in hepatocytes and endothelial cells, cytoplasm losses, vacuolization, picnotic nuclei, and mononuclear cell infiltration were identified in FA. Degeneration in chromatin material, membrane damage in mitochondria and losses in mitochondrial cristae in hepatocytes were observed in FA. We found that partially recovery in liver as a result of FA + vit E and FA + PA. We have concluded that long term use should be investigated for complete explanation of PA's protective effects on FA toxicity.

We investigated the effects of naringin on small intestine, liver, kidney and lung recovery after ischemia/reperfusion (I/R) injury of the gut. Rats were divided randomly into four groups of eight. Group A was the sham control; group B was ischemic for 2 h; group C was ischemic for 2 h and re-perfused for 2 h (I/R); group D was treated with 50 mg/kg naringin after ischemia, then re-perfused for 2 h. Endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) expressions were detected by immunolabeling. We also measured arginase activity, amounts of nitric oxide (NO) and total protein. iNOS was increased significantly in the small intestine, liver and kidney in group C. iNOS was decreased significantly only in small intestine and lung in group D. eNOS was increased significantly in the small intestine, liver and lung in group C. eNOS was decreased in small intestine, liver and lung in group D; however, eNOS was decreased in the kidney in group C and increased in the kidney in group D. The amount of NO was decreased significantly in all tissues in group D, but arginase activity was decreased in the small intestine and lung, increased in the kidney and remained unchanged in the liver in group D. The total protein increased in the small intestine and liver in group D, but decreased significantly in the kidney and lung in group D. Naringin had significant, salutary effects on the biochemical parameters of I/R by decreasing the NO level, equilibrating iNOS and eNOS expressions, and decreasing arginase activity.