Comparison of histopathologic findings of initial and recurrent lumbar disc herniation.

OBJECTIVE: Recurrent lumbar disc hernia (RLDH) is a common and challenging complication after an initial discectomy. This study aimed to investigate the relationship between the histopathologic outcomes of the initial and recurrent disc tissues. METHODS: This study investigated 70 patients who underwent a microdiscectomy and subsequently developed same-level same-side lumbar disc herniation (LDH) recurrence. The clinic, western blot, and immunohistochemical evaluations of patients with initial LDH and RLDH were conducted and statistically analyzed. RESULTS: The effect of inflammation and apoptosis in the degenerative changes of intervertebral disc hernia and increased histopathologic findings in RLDH was demonstrated. The degeneration of the hernia disc tissue is a major pathological process, which is characterized by cellular apoptosis, inflammation, and reduced synthesis of extracellular matrix. Currently, there is no clinical therapy targeting the reversal of disc degeneration. CONCLUSIONS: This, therefore, stay away from factors that increase inflammation in the intervention of intervertebral disc hernia, applying to reduce inflammation the medicines, could allow reducing disc collagen degeneration, and more successful outcomes. These findings might shed some new lights on the mechanism of disc degeneration and provide new strategies for the treatments of initial and recurrent LDH.

Effects of Quince Gel and Hesperidin Mixture on Experimental Endometriosis.

OBJECTIVES: Endometriosis (EM) is the presence of endometrial tissue outside the uterus. This study aimed to examine the effects of quince gel and hesperidin treatment on uterine tissue in an experimental endometriosis model. MATERIALS AND METHODS: Thirty-two rats were categorized into four groups as sham, EM, EM+quince gel (QG), and EM+QG+Hesperidin (HES). The endometriosis (EM) model was induced with surgical intervention. Estradiol benzoate (EB) was used to induce endometrial hyperplasia. In the EM group, EB was given to rats for 7 days. The EM+QG group received 2 cc QG for 21 days. HES treatment was given for 21 days after EM induction. At the end of the experiment, blood was taken from the animals and the serum total antioxidant status (TAS) and total oxidant status (TOS) values were studied. Uterine tissues were dissected and processed for histological paraffin embedding. Tissues were fixed in 4% glutaraldehyde solution and processed for ultrastructural analysis. RESULTS: After EM, QG and HES treatment significantly increased the TAS and decreased the TOS value. EM caused epithelial and glandular degeneration, thinning of the basal membranes, and vascular dilatation with increased fibrosis and edema. QG+HES restored the pathology and showed protective effects in uterine tissues. Caspase-3 expression was increased in the epithelium, glands, and muscle layers of the EM group. In EM+QG+HES, hesperidin protected cell survival and decreased Caspase-3 expression in uterine tissues. TNF-α expression was intense in inflammatory cells and the muscle layer in the EM group. HES reduced inflammation by decreasing the TNF-α expression. MAPK expression was increased after EM induction in epithelial, glandular, and inflammatory cells in the EM group. After HES treatment, MAPK expression was mainly negative in cells of uterine tissue in the EM+QG+HES group. Ultrastructurally, in the EM group, organelles were disrupted and dilated and degenerated after EM induction. QG and HES treatment improved cellular organelles. CONCLUSION: Local vaginal applications can be an alternative treatment method in the endometriosis model via QG+HES treatment promoting cell proliferation and angiogenesis and preventing cell death.

Evaluation of the association between biochemical and immunohistochemical score of caspase-9 and TNFα, and the grading of lumbar disc herniation.

OBJECTIVE: The aim of our study is to investigate the influence of caspase-9 and tumour necrosis factor alpha (TNFα) in the grade of lumbar disc herniation. We determined the strength of different predictors such as age, gender, disc grading, caspase-9 and TNFα. METHODS: We retrospectively reviewed 84 patients who had discectomies. Histological and biochemical evaluations of disc specimens were performed. All patients were scanned by the magnetic resonance imaging (MRI) scanner before the operation. Masson's trichrome stain, biochemical analysis and immunohistochemical staining were performed to measure the expression levels of caspase-9 and TNFα. The results were evaluated statistically. RESULTS: This study included 84 patients (mean age: 41.59 ± 12.21 years; range: 19-76): 60 men (age 40.47 ± 12.63 years) and 24 women (44.42 ± 10.81 years). No statistically significant age difference was found between the genders (p = 0.182). MRI scans showed 16 patients had protrusion, 44 had extrusion and 24 had sequestration of discs. There was a statistically significant negative correlation between the grading of lumbar disc herniations and age (p < 0.001, r = -0.509). Histological and biochemical analyses of disc materials were done. Inflammation, collagen fibre deterioration, apoptotic process, TNFα and caspase-9 were seen to increase with increasing disc grading (p < 0.01). CONCLUSIONS: Biochemical and immunohistochemical score of caspase-9 and TNFα indicate the grading of lumbar disc herniation. As the grading of disc herniation increases, inflammation of cells and collagen fibre disruption increase and accelerate the apoptotic process. Apoptosis in disc nucleus pulposus cells may reduce disc herniation.

Investigation of the effect of combined use of alloplastic-based tricalcium phosphate bone graft and antihemorrhagic plant extract (ABS) on bone regeneration in surgically induced bone defects in nondiabetic rats: an experimental animal study

Background/aim: In this experimental study, we aimed to evaluate the late period effects of the combination of Ankaferd Blood Stopper (ABS), which has bone wound healing effects, and ß-tricalcium phosphate (TCP) on the regeneration of bone tissue through histopathological, immunohistochemical, and radiological (dual energy X-ray absorptiometry - DEXA) methods in nondiabetic rats. Materials and methods: Sixty-four Wistar albino male rats were used. In the calvaria of the rats, a bone defect 7.0 mm in diameter was created. These rats were divided into 4 different groups. Group 1 was the control group without any treatment, a 0.125 mL Β-TCP graft was applied to Group 2, a 0.125 mL ABS was applied to Group 3, and a 0.125 mL (ß-TCP + ABS) mixture was applied to group 4. Half of the rats were sacrificed on day 28 and the other half on day 56. Histopathological, immunohistochemical, and DEXA analyses of the specimens were performed after the experiment. Results: As a result of the histopathological analysis, osteoblastic activity and new bone formation were found to be significantly higher in Group 2, Group 3, and Group 4 than the control group on day 28 (P < 0.05). However, inflammatory cell infiltration and vascular dilatation and hemorrhage decreased significantly compared to the control group (P < 0.05). The histopathological analysis in rats on day 56 showed that osteoblastic activity in Group 2 and Group 4 was significantly higher than in the control group, but there was a statistically significant decrease in inflammatory cell infiltration and vascular dilatation and hemorrhage compared to the control group (P < 0.05). New bone formation in Group 2, Group 3, and Group 4 was significantly higher than in the control group. Western blotting findings revealed that the osteonectin and osteopontin expression on day 28 was increased significantly in Group 2 and Group 4. DEXA analyses revealed that BMC values in Group 2 and Group 4 on day 28 were significantly higher than in the control group (P < 0.05). There was no significant difference in bone mineral density values on the 28th and 56th days (P > 0.05). Conclusion: The use of both ß-TCP + ABS and only ABS had positive effects on wound healing and bone formation in nondiabetic rats.

Evaluation of protein levels of autophagy markers (Beclin 1 and SQSTM1/p62) and phosphorylation of cyclin E in the placenta of women with preeclampsia.

Preeclampsia is a severe multisystem disorder, and its pathophysiology is still not completely understood. Autophagy, a recycling process that maintains cellular homoeostasis during differentiation and development, is controversial regarding increased or decreased autophagic activity in preeclampsia. The aim of this study was to determine whether autophagy is increased in the placentas of women with preeclampsia by examining the protein levels of autophagy markers (Beclin 1 and SQSTM1/p62) and phosphorylation of cyclin E. For this purpose, placentas from preeclampsia (n=10) and control (n=10) pregnancies were included in this study. The protein expression of autophagy-related markers Beclin1, SQSTM1/p62 and phosphorylation status of cyclin E were detected by Western blot. Our data showed that the protein levels of both Beclin 1 and SQSTM1/p62 were significantly increased, while the phosphorylation level of cyclin E was significantly decreased in placentas with preeclampsia compared to those derived from controls. The results of this study suggest that the autophagic activity is perpetually increased in preeclampsia and cyclin E protein stabilisation might be involved in the induction of autophagy.

Severe pre-eclampsia complicated by HELLP syndrome alterations in the structure of the umbilical cord (morphometric and immunohistochemical study).

The aim of this study was to evaluate the morphometric and immunohistochemistry in umbilical cords from patients with severe pre-eclampsia with and without haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome. The patient and control groups were similar according to baseline obstetric characteristics. White blood cell count in patients with HELLP syndrome and the control group was significantly increased among patients with HELLP syndrome (p < 0.001). Morphometric examination and endothelial core length were significantly different between the groups. In the umbilical cord cross-section of the HELLP group, endothelial cell degeneration in the vessel wall and basement membrane thickening were observed. In the muscle layer of blood vessels, the following disorders were found: increased collagen fibres in the muscle cell, hyperplasia and separation of muscle fibres as well as edema in the intermediate connective tissue. Immunohistochemical analysis showed that endothelial cells, basal membrane and fibroblast cells in the HELLP group expressed high levels of CD44. Vessel wall and amniotic epithelial basement membrane thickening were observed in the HELLP group. Matrix metalloproteinase 9 (MMP9) was expressed. Fibroblast and smooth muscle cells were fusiform and showed a positive reaction to immunohistochemical staining of α-actin smooth muscle.

Ellagic acid protected the gingival tissue via fibroblast and epidermal growth factors in rats.

PURPOSE: To investigate the effect of ellagic acid (EA) in gingival tissues injury in rats. METHODS: Twenty rats were categorized into two groups. In burn group, an excisional wound area was created by removing a 4-mm diameter flap from the left molar region in the mucoperiosteal region of the gingiva. In burn + ellagic acid group, 1.2 mg/mL EA was administered as irrigation for one week. Animals was sacrificed under anesthesia at the end of experiment. Malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) level were measured. Hematoxylin and eosin, fibroblast growth factor (FGF) and epidermal growth factor (EGF) immunostainings were applied to tissues. RESULTS: MDA, MPO, inflammation and leukocyte infiltration were high in burn group. Degeneration epithelium, edema and inflammatory cell infiltration in connective tissue areas, and dilatation and congestion in blood vessels were observed in burn group. In burn + EA group, the gingival epithelium improved, collagen fiber production increased and organized dermis were observed. After burn injury, FGF and EGF activity was increased in EA treated groups. CONCLUSIONS: We suggest that EA have the potential for better healing outcomes in oral wounds. EA seems to have promising therapeutic efficacy to enhance oral wound healing.

E-cadherin and NF-κB expression in the vagina after ovarian ischemia and reperfusion.

PURPOSE: To investigate inflammation and cell adhesion molecules in the vagina after ovarian ischemia-reperfusion (IR) injury. METHODS: 20 Wistar albino female rats were divided into two groups: control, and IR groups. In IR group, blood flow was restricted for 2 hours for ovarian ischemia. Then, tissues were re-blood 2 hours for reperfusion. Vagina tissues were excised and processed for histopathological analysis. Histopathological and biochemical follow-ups were performed. RESULTS: Both malondialdehyde and myeloperoxidase values were increased in IR group compared to control group. Glutathione content was decreased in IR group compared to control group. Epithelial degeneration, inflammation, dilatation, and nuclear factor-κB (NF-κB) expression were increased in IR group compared to control group. E-cadherin expression was significantly decreased in IR group. In the IR group, E-cadherin showed a positive reaction in adenomas, gland-like cryptic structures, cellular junctions with clustered inflammatory cells. In the IR group, NF-κB expression was increased in basement membrane, inflammatory cells, in blood vessels. CONCLUSIONS: Ovarian ischemia caused degeneration of epithelial cells in the vaginal region and disruptions in the cell junction complex, which leads to activation of E-cadherin and NF-κB signaling pathway and alterations in reproductive and embryonal development in the vaginal region.

Investigation of the histopathological level of Ki-67, caspase-3 expressions of the effects of hesperidin on wound healing in the rat esophagus.

PURPOSE: The effects of hesperidin application on the wound caused by esophageal burns were investigated in this study. METHODS: Wistar albino rats were divided into three groups: Control group: only 1 mL of 0.09% NaCl was administered i.p. for 28 days; Burn group: An alkaline esophageal burn model was created with 0.2 mL of 25% NaOH orally by gavage-1 mL of 0.09% NaCl was administered i.p. for 28 days; Burn+Hesperidin group: 1 mL of 50 mL/kg of hesperidin was given i.p. for 28 days to rats after burn injury. Blood samples were collected for biochemical analysis. Esophagus samples were processed for histochemical staining and immunohistochemistry. RESULTS: Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were significantly increased in Burn group. Glutathione (GSH) content and histological scores of epithelialization, collagen formation, neovascularization was decreased. After hesperidin treatment, these values were significantly improved in the Burn+Hesperidin group. In the Burn group, epithelial cells and muscular layers were degenerated. Hesperidin treatment restored these pathologies in Burn+Hesperidin group. Ki-67 and caspase-3 expressions were mainly negative in control group; however, the expression was increased in the Burn group. In the Burn+Hesperidin group, Ki-67 and caspase-3 immune activities were reduced. CONCLUSIONS: Hesperidin dosage and application methods can be developed as an alternative treatment for burn healing and treatment.

Histopathological, ultrastructural, and immunohistochemical examination of changes in the placenta as a result of severe preeclampsia.

PURPOSE: To investigate the role of hypoxia-inducible transcription factor-1 alpha (HIF-1α) and angiogenetic factor endothelin-1 (ET-1) expression in regulating hypoxia and placental development by routine histopathological methods. METHODS: Twenty preeclamptic and normal placentas were used. Placenta tissue pieces were examined histopathologically after routine paraffin follow-ups. HIF-1α and ET-1 proteins were examined immunohistochemically, and placental tissues were examined ultrastructurally. RESULTS: Increase in syncytial proliferation, endothelial damage in vessels, and increase in collagen were observed in preeclamptic placentas. As a result of preeclampsia, an increase was observed in HIF-1α and ET-1 protein levels in the placenta. Dilatation of endoplasmic reticulum and loss of cristae in mitochondria were observed in trophoblast cells in preeclamptic placental sections. CONCLUSIONS: High regulation of oxygen resulting from preeclampsia has been shown to be a critical determinant of placentagenesis and plays an important role in placental differentiation, changes in maternal and fetal blood circulation, trophoblastic invasion, and syncytial node increase. It has been thought that preeclampsia affects secretion by disrupting the endoplasmic reticulum structure and induces mitochondrial damage, and that ET-1 may potentially help in the induction of stress pathways as a result of hypoxia in preeclampsia.

Role of SOX9 and Hif-1α expression in placentas of patients with HELLP.

PURPOSE: In this study, we investigated the immunohistochemical staining of SRY-box transcription factor 9 (SOX9) and Hif-1α expression in placentas of pregnant woman with hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome. METHODS: Placentas of 20 normotensive 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 SOX9 and Hif-1α immunostaining. RESULTS: Normotensive placentas showed normal histology of placenta, however placentas of HELLP syndrome showed intense thrombosis, thinning of the villi membrane and vascular dilatation. In placentas of normotensive patients, SOX9 reaction was immunohistochemically negative, however placentas of HELLP group showed SOX9 expression in decidual cells, and syncytial regions of floating villi and inflammatory cells. In placentas of normotensive patients, Hif-1α reaction was mainly negative in vessels and connective tissue cells. Placentas of HELLP group showed increased Hif-1α expression in decidual cell and especially inflammatory cells in the maternal region. CONCLUSIONS: Hif-1α and SOX9 proteins can be used as a marker to show severity of preeclampsia and regulation of cell proliferation and angiogenesis during placental development.

Investigation of Beclin 1 and TNF-α expressions in preeclampsia placentas: Immunohistochemical study.

BACKGROUND: Preeclampsia is a pregnancy complication Aim of this study was to investigate expression of Beclin1 and tumor necrosis factor (TNF)-α in normotensive and preeclamptic placentas of pregnant women patients. METHODS: Twenty normotensive and 20 preeclamptic patients placentas were dissected for paraffin- wax processing. Placental samples were embedded in parafin blocks. Sections were stained with Hematoxylin-Eosin staining and TNF-α and Beclin1 immunostaining. RESULTS: In control group, root and floating villi were normal in histological perspectives, syncytial node number was low, vessels were normal with connective tissue. No hemorrhage was observed in the intervillous area. In preeclampsia group, decidual cell degeneration and fibrinoid accumulation increased. Vascular dilatation and congestion with mononuclear cell infiltration were observed. Beclin1 reaction was generally negative in control group. In preeclampsia group, Beclin1 reaction was increased in decidual cells, syncytial nodes and bridges and in chorionic villi and in some Hoffbauer cells. In control group, TNF-α expression was mainly negative but only in some decidual cells. In preeclampsia, TNF-α reaction was observed in degenerated decidua cells, in leukocytes and in villi. CONCLUSION: In preeclampsia placentas, degenerated decidua cells and inflammation increased. It was thought that Beclin1 and TNF-α signals could be used as a marker in affecting the fetal structure of blood flow in preeclamptic placentas.

Biochemical and immunohistochemical examination of the effects of ephedrine in rat ovary tissue.

PURPOSE: It was aimed to investigate the biochemical and immunohistochemical effects of ephedrine (EPH) in bilateral ovariectomized rats. METHODS: Twenty-four Sprague Dawley female rats were divided into three groups: control group: The abdomen was opened and closed without any treatment; ischemia-reperfusion (IR) group: 2 h of ischemia followed by 2 h of reperfusion were allowed to cause IR injury; IR+EPH group: oral EPH solution (5 mg/kg) was administered for 28 days. RESULTS: Biochemical parameters were statistically significant in group comparisons. Increased interleukin-6 (IL-6) expression, degenerative preantral and antral follicle cells and inflammatory cells around blood vessels were seen in IR group. Negative IL-6 expression was observed in seminal epithelial cells, preantral and antral follicle cells in IR+EPH group. While caspase-3 activity increased in granulosa cells and stromal cells in IR group, caspase-3 expression was negative in preantral and antral follicle cells in the germinal epithelium and cortex in IR+EPH group. CONCLUSIONS: The effect of apoptosis, which occurs with the signaling that starts in the cell nucleus, caused the cessation of the stimulating effect at the nuclear level after EPH administration, and a decrease in the antioxidative effect in IR damage and inflammation in the apoptotic process.

Protective effect of nebivolol on rat ovary exposed to deltamethrin toxicity.

PURPOSE: We aimed to investigate the antioxidant activity of nebivolol against possible damage to the ovarian tissue due to the application of deltamethrin as a toxic agent, by evaluating histopathological proliferating cell nuclear antigen (PCNA) and tumor necrosis factor-alpha (TNF-α) signal molecules immunohistochemically. METHODS: The animals were divided into three groups as control, deltamethrin and deltamethrin + nebivolol groups. Vaginal smears were taken after the animals were mated and detected on the first day of pregnancy. After the sixth day, deltamethrin (0.5 mL of 30 mg/kg BW undiluted ULV), and 2 mL of sterile nebivolol solution were administered intraperitoneally every day for 6-21 periods. After routine histopathological follow-up, the ovarian tissue was stained with hematoxylin and eosin stain. RESULTS: Control group showed normal histology of ovarium. In deltamethrin group, hyperplasic cells, degenerative follicles, pyknotic nuclei, inflammation and hemorrhagic areas were observed. Nebivolol treatment restored these pathologies. Deltamethrin treatment increased TNF-α and PCNA reaction. However, nebivolol decreased the expression. CONCLUSIONS: It was thought that deltamethrin toxicity adversely affected follicle development by inducing degeneration and apoptotic process in preantral and antra follicle cells, and nebivolol administration might reduce inflammation and slow down the apoptotic signal in the nuclear phase and regulate reorganization.

Effects of daidzein on rat ovary against ischemia-reperfusion.

PURPOSE: Our aim was to investigate protective effects of daidzein treatment on ischemia-reperfusion (I/R) injury-induced ovarian tissue by immunohistochemical techniques. METHODS: Thirty Sprague Dawley female rats were categorized into three groups as sham, I/R group, and I/R+daidzein groups. Bloods were analyzed for malondialdehyde (MDA), glutathione peroxidase (GSH), and myeloperoxidase (MPO), and ovaries were processed for histological tissue protocol. RESULTS: Both MDA and MPO values were increased in I/R group compared to sham and I/R+daidzein groups. GSH content was increased in I/R+daidzein group compared to I/R groups. In I/R group, theca and follicular cells were degenerated with apoptosis and dilatation and congestion, edema. In I/R+daidzein group, daidzein improved pathologies. In the I/R group, Bax expression was positive with follicular cells, granulosa cells and inflammatory cells. In the I/R+daidzein group, positive Bax reaction was observed in the epithelial, antral, and inflammatory cells. In I/R group, Bcl-2 reaction was in germinative epithelial cells, cells of antral follicle. In the I/R+daidzein group, Bcl-2 expression level was reduced after daidzein treatment. CONCLUSIONS: After the I/R procedure, ovarian cells and follicles were degenerated with apoptosis and inflammation. After daidzein treatment, Bax and Bcl-2 signal were decreased. It was observed that daidzein stopped the apoptotic process.

Severe preeclampsia complicated by HELLP syndrome alters the structure of Hofbauer and syncytiotrophoblast cells: ultrastructural and immunohistochemical study.

Background: Hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome is generally considered to be a variant or complication of preeclampsia. It is a life-threatening obstetric complication. Objectives: To evaluate the immunohistochemistry and ultrastructural of syncytiotrophoblastand Hoffbauer cells in placental villi of patients with HELLP syndrome. Methods: Two groups of patients with a total of 50 full-term human placentas (n = 25 in each group) were assigned as the control (normotensive) and HELLP syndrome. Placental tissue samples were fixed in 10% neutral formalin and paraffin-embedding protocol was performed. We prepared 5 µm sections for histological and immunohistochemical staining. Sections were immunostained with Hoffbauer cell marker CD68. For transmission electron microscopy (TEM), placental tissue samples were fixed in 2.5% buffered glutaraldehyde and then, in 1% osmium tetroxide for routine ultrastructural examinations. Results: When the HELLP group fetal placental sections were examined, intracytoplasmic edema in syncytiotrophoblast, degenerative vacuoles, and degenerative findings on cell surface membranes were observed. Moreover, villous edema was remarkable. The number of CD68-positive Hoffbauer cells per villus control group sections was 0.23 ± 0.02 and the number of CD68-positive cells per villus in HELLP group placenta sections was 0.83 ± 0.12. The increase in the number of Hoffbauer cells per villus in the HELLP group was significant (P < 0.001). Compared with the control group, there was a significant increase in the number of Hoffbauer cells and syncytiotrophoblasts in the HELLP group, and degenerative changes were also observed in the ultrastructure of these cells. Conclusions: Pathology of the HELLP syndrome is in relation to CD68-positive placental macrophages.

Histopathological, immunohistochemical and biochemical alterations in liver tissue after fungicide-mancozeb exposures in Wistar albino rats.

PURPOSE: To evaluate the histopathological, immunohistochemical, and biochemical effects of liver changes after mancozeb administration. METHODS: Rats were divided into groups-the control group (n=7) and the mancozeb group (n=7)-, given 500 mg/kg mancozeb dissolved in corn oil daily for four weeks by an orogastric tube. Caspase-3 and tumor necrosis factor-alpha (TNF-α) primary antibodies were used for immunohistochemical analysis. RESULTS: Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values of the mancozeb group increased significantly than ones of the control group. Venous dilatation, inflammation, hepatocyte degeneration, TNF-α, and caspase-3 expression scores increased significantly in the mancozeb group. In the mancozeb group, intensive caspase-3 expression was observed in hepatocyte cells around the central vein in the center of the liver lobule, and there was an increase in TNF-α expression in the inflammatory cells around the enlarged central vein and Kupffer cells and apoptotic hepatocyte cells. CONCLUSIONS: Subacute mancozeb exposure in rats leads to elevated toxicity with impaired liver function, increased inflammation in tissue and increased apoptosis due to cellular damage in the liver, and decreased liver regeneration ability due to congestion and degeneration of blood vessels.

Hepatotoxic effects of melamine exposure from the weaning period in rats: a flow cytometric, electron microscopic, and histopathologic study.

This study aims to investigate the effects of melamine exposure from the weaning period (21st postnatal days in rats) on liver tissue. Female Wistar albino rats (n = 18) were divided into three groups. About 0.1-ml saline was applied to the control group by gavage for 21 days from the postnatal 21st day. The second group was taken 50-mg/kg melamine (in 0.1-ml saline) and the third group was taken 75-mg/kg melamine (in 0.1-ml saline) p.o. On the postnatal 45th day, all rats were sacrificed under anesthesia. Then, liver tissues were cut into three parts and two of them placed in neutral formalin for histopathological and flow cytometric analysis, and one of them placed in 2.5% glutaraldehyde. Histopathological analysis was performed with hematoxylin & eosin, Masson trichrome, periodic acid Schiff stained sections, and also with transmission electron microscopy. Apoptosis (Annexin V positivity) was analyzed by flow cytometry. According to histopathological analysis, hepatocyte damage, sinusoidal dilatation, and inflammatory cell infiltration significantly increased in both melamine groups compared with the control group. Apoptosis significantly increased in the 50 and 75-mg melamine groups compared with the control group. In the results of transmission electron microscopy analysis, there was abnormal chromatin distribution in the hepatocyte nuclei, loss in the cristae of the mitochondria, and organelle loss in large areas in the cytoplasm in both melamine exposure groups. As result, melamine exposure from the weaning period causes liver damage with increasing doses.

The effect of rosmarinic acid on deformities occurring in brain tissue by craniectomy method. Histopathological evaluation of IBA-1 and GFAP expressions.

PURPOSE: To investigate the role of Rosmarinic acid (RA) in the prevention of traumatic brain injury and the immunohistochemical analysis of IBA-1 and GFAP expressions. METHODS: Healthy male rats were randomly divided into 3 groups consisting of 10 rats. Groups were as follows; control group, traumatic brain injury (TBI) group, and TBI+RA group. After traumatic brain injury, blood samples were taken from the animals and analyzed with various biochemical markers. And then IBA-1 and GFAP expressions were evaluated immunohistochemically. RESULTS: Significant results were obtained in all biochemical parameters between groups. Immunohistochemical sections showed IBA-1 not only in microglia and macrophage activity but also in degenerative neurons in blood vessel endothelial cells. However, GFAP reaction and post-traumatic rosmarinic acid administration showed positive expression in astrocytes with regular structure around the blood vessel. CONCLUSION: Rosmarinic acid in blood vessel endothelial cells showed that preserving the integrity of astrocytic structure in the blood brain barrier may be an important antioxidant.

Short-term use of resveratrol in alloplastic graft material applied with calvarial bone defects in rats.

PURPOSE: The effects of resveratrol administration on calvarial bone defects with alloplastic graft material was investigated for osteoinductive reaction and bone development in rats. METHODS: Healthy male rats were randomly divided into 3 groups consisting of 10 rats. Groups were as follows: control (defect) group, defect + graft group, and defect + graft + resveratrol group. A calvarial bone defect was created in all groups, alloplastic bone grafts were applied to the defect in the 2nd and 3rd group, resveratrol (5 mg/kg/day) was added to the drinking water of the animals following graft application for 28 days in the 3rd group. RESULTS: Increase in osteoclasts and necrotic changes were observed histopathologically in the control group. In the 2nd group, reduction of inflammation, congestion of blood vessels, increased osteblastic activity, osteoinductive effect, progression of osteocyte development and increased collagen fibers in connective tissue were observed. In the 3rd group, osteoblasts seemed to secrete bone matrix and accelerate osteoinductive effect with increased osteopregenitor activity and positive osteopontin and osteonectin expressions. CONCLUSION: Resveratrol treatment was thought to be an alternative and supportive drug for implant application by inducing new bone formation in the calvaral defect region as a result of short-term treatment.