Protective effects of Silymarin on testicular torsion/detorsion in rats.

OBJECTIVE: The present research aimed to study the possible protective effects of Silymarin on testicular I/R injury in a rat model evaluated through histopathology and biochemical parameters. MATERIALS AND METHODS: This research investigated the impact of Silymarin on IR damage in male Wistar albino rats. Animals were divided into three groups: group 1 (sham), group 2 (IR), and group 3 (IR+Silymarin). RESULTS: There were no notable differences in the levels of malondialdehyde (MDA), myeloperoxidase (MPO), and glutathione (GSH) across the three groups (p=0.260, p=0.486 and p=0.803, respectively). Contrarily, the total antioxidant status (TAS) levels exhibited significant variations between groups (p=0.001). The total oxidant status (TOS) levels also differed significantly between groups (p=0.004). The tissue evaluations uncovered substantial differences in the Johnson score, which is used to gauge testicular damage. A distinct contrast was seen between Group 1 and Group 2, and also between Group 2 and Group 3, with an all-encompassing p-value lower than 0.01. The same significant disparities were found for the percentages of Bax and Annexin V immunostaining (p<0.01 for each), reflecting the inflammation and apoptosis brought about by ischemia-reperfusion and the protective effects of the treatment. CONCLUSIONS: The outcomes of the current investigation showed that Silymarin could be a valuable agent for reducing testicular tissue damage following I/R injury.

Protective effectiveness of anise against testicular ischemia and reperfusion injury: An experimental study in rats.

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.

Immune activity of Ki-67 during nasal polyp development.

OBJECTIVE: Nasal polyps are non-cancerous, soft painless growth of nasal mucosa. In this study, our aim was to investigate the Ki-67 expression level in nasal polyps by immunohistochemical method. PATIENTS AND METHODS: 30 patients with nasal polyps were included in this study. Nasal polyps were processed for paraffin wax embedding protocol. Samples were fixed and embedded in paraffin blocks. 5 µm sections were stained with Hematoxylin-Eosin dye and immune stained with Ki-67 antibody. Sections were analyzed under light microscope. RESULTS: Blood parameters showed that white blood cells, hematocrit and platelet were higher than normal range. In sections of hematoxylin-eosin staining, elevated basal cells, thin basement membrane, leukocyte infiltration, collagen fibers degeneration were observed. Masson trichrome staining revealed that degenerative epithelial cells, detached basement membrane and edema were observed. Ki-67 expression was observed in mucosal epithelial cells, vascular endothelial cells and plasma cells in immune staining. CONCLUSIONS: Epithelial degeneration in nasal polyps and leukocyte infiltration induce nasal adenoma. Ki-67 expression may be a diagnostic tool for epithelial leukocyte formation.

Role of cited-1 and caspase-6 expression in HELLP syndrome.

OBJECTIVE: In this study, we investigated the immunohistochemical staining of cited-1 and caspase-6 expression in the placentas of pregnant women with HELLP syndrome. PATIENTS AND METHODS: Placentas of 20 normotensive patients and 20 women with HELLP syndrome were processed for routine histological tissue processing. The biochemical and clinical parameters of patients were recorded. Placentas were stained with hematoxylin-eosin and cited-1 and caspase-6 immunostaining. RESULTS: Placentas of normotensive patients showed normal histology. Placentas of women with HELLP syndrome showed degenerated cells, hyalinization and vacuolization. Cited-1 expression was negative in normotensive group; however, it was increased in HELLP group, especially in decidual cells, endothelial cells and other placental cells. Caspase-6 expression was negative in placental structures of normotensive groups. However, it was intense in decidual cells, vacuolar and hyalinized areas, inflammatory cells and connective tissue cells in HELLP group. CONCLUSIONS: Cited-1 and caspase-6 are a marker in determining the severity of HELLP syndrome.

Momordica charantia reduced ovarian ischemia - reperfusion injury by suppressing APAF-1 expression.

OBJECTIVE: We investigate the effect of Momordica charantia (MC) against ovarian ischemia-reperfusion injury (IRI). MATERIALS AND METHODS: Forty-eight Sprague Dawley female rats were divided into 6 groups. 3 hours ischemia/3 hours reperfusion was conducted. Before and/or after IR, 600 mg/kg MC were introduced to rats via an orogastric tube. At the end of the experiment, total serum antioxidant/oxidant status (TAS/TOS) and Anti-Mullerian Hormone (AMH) level were measured. Ovarian histopathology and APAF-1 expression level were analyzed. RESULTS: TAS and AMH levels were the lowest, while TOS level and OSI were the highest in the IR group. TAS and AMH levels were higher, and TOS levels and OSI were lower in MC-treated groups compared to IR group. Follicular degeneration, granulosa and stromal cell degeneration, mononuclear cell infiltration and vascular congestion and dilatation were observed in the IR group. Ovarian histopathology was improved in groups that received MC extract. APAF-1 immune activity was intense in IR and MC+IR groups while decreased in the groups treated with MC extract after IRI. MC treatment downregulated APAF-1 protein after IRI. CONCLUSIONS: MC extract restored negative biochemical and histochemical changes caused by IRI due to its antioxidant properties and supported cell survival by suppressing APAF-1 expression.

Daidzein alleviated the pathologies in intestinal tissue against ischemia-reperfusion.

OBJECTIVE: The aim of this study was to investigate the effect of daidzein against intestinal ischemia-reperfusion injury in rats. MATERIALS AND METHODS: Thirty male Wistar albino rats with a mean weight of 200-250 gr were used. Animals were categorized into sham, ischemia-reperfusion (IR), and IR+Daidzein group. 3-hour ischemia of intestine was created by occluding superior mesenteric artery and then left for 3-hour reperfusion. In IR+daidzein group, after ischemia, 50 mg/kg daidzein was orally administered to the animals. Blood samples were collected for biochemical assays. Intestine tissues were excised for histopathologic and immunohistochemical processing. RESULTS: Malondialdehyde (MDA) increased, and Catalase (CAT) and Glutathione (GSH) decreased after IR in intestine tissue. Daidzein treatment decreased MDA and increased CAT and GSH level in IR+Daidzein group. Histopathologically, sham group showed normal intestinal tissue histology. In IR group, epithelial and villi degeneration, edema, leukocyte infiltration, vascular dilatation and congestion was observed. After Daidzein treatment, these pathologies were improved. The caspase-6 expression was mainly negative in sham group. After IR, caspase-6 reaction was very high in IR group. Daidzein reduced caspase-6 expression in IR+Daidzein group. Ki67 immune staining was negative in the sham group. In IR group, Ki67 expression was increased in inflammatory cells, deep glandular cells and in some goblet cell nuclei. In IR+Daidzein group, Ki67 expression was decreased due to reduced inflammation. CONCLUSIONS: IR injury causes oxidative stress, apoptosis and inflammation. Daidzein treatment improved histopathology against intestinal IR.

Effect of ellagic acid on damage caused by hepatic ischemia reperfusion in rats.

OBJECTIVE: Ischemia (I) causes lack of oxygen delivery to the tissues, leading to hypoxia and cellular damage. Reperfusion (R) is the re-blooded of the tissue; however, it may cause more tissue damage than ischemia alone in some cases. During IR, number of free radicals and metabolic by-products increases. To prevent this, cellular antioxidant system is activated but it may not be enough to restore the cellular activities. The aim of this study was to investigate the potential protective effect of Ellagic Acid on damage caused by hepatic IR in rats. MATERIALS AND METHODS: Thirty rats were divided into three groups: (1) Sham group - no drug administration but only midline laparotomy was performed in the abdomen; (2) Ischemia-Reperfusion (IR) group - ischemia was applied for 1 hour by sealing the portal vein and hepatic artery, then vessels were reperfused for 6 hours; (3) IR+Elagic Acid (EA) group - after IR, 10 mg/kg of EA was given intraperitonially to the rats once a day for 28 days. Oxidative stress markers were analyzed by blood collection. Hepatic tissues were processed for histological and immunohistochemical analysis. RESULTS: MDA level and MPO activity were increased and GSH content was decreased after IR group was compared to sham group. After EA treatment, these values were improved in IR+EA group. IR caused hepatocyte degeneration, sinusoidal dilatation, leukocyte infiltration and disintegrity of hepatic tissue. EA administration improved histopathology after IR. IR injury increased TNF-α and Caspase-9 expression in hepatocytes and vascular endothelial cells in IR group; however, both decreased in EA-received group. CONCLUSIONS: Ellagic Acid may reduce oxidative stress level and prevent induction of inflammation and cell death against hepatic IR.

Vitamin E protected the mouse adrenal gland against immobilization stress.

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.