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In this study, we aimed to investigate the effects of vitamin E on mouse adrenal glands in immobilization stress. Twenty-eight male, 10-week-old, BALB/C mice weighing 30-45 grams were divided into four groups. Mice were placed in a cage where no movement was allowed 6 hours/day for 7 days for immobilization stress. 10 ml/kg vitamin E was administered orogastrically 1 hour before immobilization stress in the vitamin E and stress+vitamin E group. At the end of the 7th day, all the animals were subjected to elevated-plus maze (anxiety) and forced swimming (depression) tests. Left adrenal glands were dissected for routine paraffin tissue embedding protocol. Adrenal sections were stained with hematoxylin-eosin and Azan. Malonaldehyde (MDA) levels were also measured in the adrenal tissues. Anxiety level (0.023), depression level (p=0.042) and MDA values (p=0.01) were significantly increased in the stress group. Histological sections of the stress group showed cortical atrophy, medullary hypertrophy, vascular dilation and hemorrhage. Azan staining revealed a thinned capsule and corticomedullary fibrosis in the stress group. Pathologies induced by immobilization stress were mostly reversed after vitamin E administration. The results suggested that vitamin E alleviates adverse effects of immobilization stress (oxidative, behavioral and histopathologic changes) in mice.
Nicotine, the main toxic component of tobacco, directly or indirectly causes adverse effects on the liver metabolism. Melatonin, secreted by the pineal gland, has anti-apoptotic activity as well as antioxidant activity. The aim of this study was to reveal the antiapoptotic effects of melatonin in rats with experimentally induced chronic liver damage with nicotine. In this study, 32 male Wistar albino rats were divided into four groups: control, melatonin, nicotine and nicotine+melatonin. During the experiment, nicotine (1 mg/kg) and melatonin (10 mg/kg) were administered daily intraperitoneally for 56 days. At the end of the study, the liver tissues were taken for histopathological, immunohistochemical and molecular analysis. The administration of melatonin was determined to partially alleviate histopathological changes in the liver tissue induced by nicotine, such as hepatocyte degeneration, vascular dilatation and congestion, and leukocyte infiltration. It was observed that there was a significant decrease in Bax expression levels and a significant increase in Bcl-2 expression levels in the nicotine+melatonin group when compared to the injury group. On the other hand, it was determined that melatonin administration reduced the Bax/Bcl-2 ratio, which was significantly higher in the nicotine group compared to the other groups, to a level close to the control group. Additionally, as a result of immunohistochemical evaluation, it was observed that decreased Bax expression and increased Bcl-2 expression in hepatocytes in the nicotine+melatonin group were at a level close to the control group. Our results revealed that melatonin is a hepatoprotective and effective antioxidant by suppressing cell apoptosis and increasing the rate of healing after damage at both the immunohistochemical and molecular levels.
Intestinal ischemia-reperfusion (IR) injury is a major clinical challenge due to its high morbidity and mortality rates. This study aims to demonstrate the effect of honokiol, a natural antioxidant compound, on intestinal IR injury in rats using histochemical and biochemical methods. The protein-protein interaction (PPI) network construction and the honokiol-target network-reactome pathway analysis were performed using Cytoscape v3.10.1 software to validate inclusion of focused proteins in the study. 1 hour/2 hours of IR was applied on intestinal (jejunum) tissues. The tissues were further processed for biochemical measurement of total oxidant status (TOS) and antioxidant status (TAS). 5 mg/kg honokiol treatment was administered to rats after ischemia protocol. The tissues were fixed in formaldehyde and embedded in paraffin protocol. Sections were stained with vascular endothelial growth factor (VEGF), a disintegrin and metalloproteinase with thrombospondin motifs 15 (ADAMTS-15) and caspase-3 antibodies. Analysis of the signaling network revealed that honokiol exerts a significant influence on the proposed mechanisms associated with IR through the VEGF, ADAMTS-15, and caspase-3 network. IR increased the TOS level and decreased the TAS level in ischemia and IR group, histopathologically damaged the intestinal tissues and led to epithelial degeneration, increased cell death, vascular dilatation and congestion. Honokiol treatment reduced the oxidant enzymes and supported the antioxidant system, and restored pathologies in the IR+honokiol group. Intestinal IR injury increased VEGF expression, ADAMTS-15 and caspase-3 expression in the ischemia and IR groups. Honokiol treatment after ischemia reduced the VEGF, ADAMTS15 and caspase-3 by restoring tissue integrity, preventing cell death and increasing cell matrix remodeling. The administration of honokiol provided protection against intestinal IR injury by modulating apoptosis, angiogenesis, extracellular matrix remodeling processes through regulation of the VEGF, ADAMTS-15, and caspase-3 expression.
Testicular torsion is a frequently encountered clinical condition that requires urgent treatment. The aim of this study is to investigate the efficacy of Anise (Pimpinella anisum L.) in treating the pathological condition due to ischemia and reperfusion injury by using biochemical, histopathological and immunohistochemical methods. A total of 6 groups were formed with 8 male Wistar Albino rats in each group. Group 1 (n=8): control group, Group 2 (n=8): Anise aqueous solution was given orally 5 ml/kg by gavage for 30 days. Group 3 (n=8): Ischemia and Reperfusion (I/R) group, bilateral testicles were rotated 270° and reperfused after 30 minutes of ischemia. Group 4 (n=8): I/R+ Anise group, Group 5 (n=8): Anise+ I/R group and Group 6 (n=8): Anise+ I/R+ Anise group. The results of the Anise group and the Control group were similar. However, the damage in the I/R group was considerably more severe than in any of the other study groups. While it was observed that spermatogenic cells started to regenerate in the I/R+Anise group, edema and congestion were observed in the Anise+I/R group. In the Anise+I/R+Anise group, all histological findings and biochemical parameters were similar to those of the control group. It was observed that anise had protective effects in ischemia and reperfusion injury in rat testicles.
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