Histopathological evaluation of IBA-1, GFAP activity in the brain cortex of rats administered cadmium chloride.

Purpose: This study aims to evaluate the changes in brain tissue and blood-brain barrier due to oxidative stress during cadmium (Cd) poisoning by biochemical, histopathological, and immunohistochemical methods. Methods: 170-190 g weighing eight-week-old female Wistar albino rats were divided into two groups (control and experimental), with 7 animals in each group. Experimental group rats were given 2 mg/kg/day powdered cadmium chloride dissolved in water intraperitoneally every day for two weeks. Biochemical, histopathological and immunohistochemical examination was performed. Results: It was seen that brain malondialdehyde (MDA) levels increased significantly, and glutathione (GSH) and catalase (CAT) activity levels decreased. In addition to degeneration in some pyramidal cells and glial cells, deformity, and picnosis in the nucleus, dilation of the meninges and cortex vessels, and inflammation around the blood vessels were observed. An increase was found in ionized calcium binding adaptor molecule 1 (IBA-1) expression in microglia cells and degenerative endothelial cells, and increased glial fibrillary acidic protein (GFAP) expression was observed in astrocytes and degenerate neurons. Conclusions: It has been shown that cadmium toxicity may cause microgliosis and astrogliogenesis by inducing cytokine production due to cell degeneration, vascularity, and inflammation in the brain cortex and by affecting microglia, astrocytes cells.

Proflactic effects of rosmarinic acid on spinal cord injury in rats.

PURPOSE: Spinal cord injury (SCI) causes various neurological consequences that disrupt the structure of axons. The C/EBP Homologous Protein (CHOP) acts in neuronal death by apoptosis has been demonstrated in experimental models. Rosmarinic acid (RA) is a phenolic compound used for therapeutic purposes in many diseases. In this study, we investigated the therapeutic effect of Rosmarinic acid application on inflammation and apoptotic development after spinal cord injury. METHODS: Male Wistar albino rats (n: 24) were assigned to three group: control, SCI and SCI+ RA. All rats were fixed on the operating table after anesthesia, the skin of the thoracic region was opened with a midline incision and the paravertebral muscles were dissected and T10-T11 laminas were exposed. A cylindrical tube of 10 cm length was fixed to the area to be laminectomy. A metal weight of 15 grams was left down the tube. Spinal damage was created, skin incisions were sutured. 50 mg/kg rosmarinic acid was given orally for 7 days after the spinal injury. Spinal tissues were fixed in formaldehyde solution and processed for paraffin wax tissue protocol and 4-5 µm sections were taken with microtome for further immunohistochemical examination. Caspase-12 and CHOP antibodies were applied to sections. Remaining tissues were carried out in glutaraldehyde for the first fixation then in osmium tetroxide for the second. Tissues were kept in pure araldite and thin sections were taken for transmission electron microscope. RESULTS: Values of malondialdehyde (MDA), myeloperoxidase (MPO), glutathione peroxidase (GSH), neuronal degeneration, vascular dilation, inflammation, CHOP and Caspase-12 expression were increased in SCI group compared to control group. Only glutathione peroxidase content was decreased in SCI group. In SCI group, disruption of basement membrane structure in canalis ependymalis, degeneration in structures of unipolar bipolar and multipolar neurons, and apoptotic changes were seen with increased inflammation in the piamater region and positive CHOP expression in vascular endothelial cells. In SCI+RA group, reorganization of basement membrane pill in canalis ependymalis were observed with mild Caspase-12 activity in some canalis ependymal and glial cells. Also, moderate CHOP expression in multipolar and bipolar neurons and glia cells were observed. CONCLUSIONS: The application of RA has a significant effect on preventing damage in SCI. It was thought that CHOP and Caspase-12 mediated oxidative stress could be a guide in showing the potential and therapeutic target to stop the apoptotic course after SCI injury.

Effects of thymoquinone on spinal cord injury in rats.

PURPOSE: Spinal cord injury (SCI) is a condition that causes disturbances in normal sensory, motor, and autonomic functions. During SCI, damages occur such as, contusion, compression, distraction. The aim of this study was to investigate effects of the antioxidative thymoquinone on neuron and glia cells in SCI biochemically, immunohistochemically and ultrastructurally. METHODS: Male Sprague-Dawley rats were divided into Control, SCI and SCI + Thymoquinone groups. After T10- T11 laminectomy was performed, a metal weight of 15 grams was left down the spinal tube for spinal damage. Immediately after the trauma, the muscles and skin incision were sutured. Thymoquinone was given to the rats by gavage as 30mg/kg/21days. Tissues fixed in 10% formaldehyde, embedded in paraffin wax and immunstained with Caspase-9 and phosphorylated signal transducer and activator of transcription 3 (pSTAT-3) antibodies. Remaining were stored at -80oC for biochemistry. Frozen spinal cord tissues were placed in a phosphate buffer solution and homogenized, centrifuged then used to measure malondialdehyde (MDA) levels, glutathione peroxidase (GSH) and Myeloperoxidase (MPO). RESULTS: In the SCI group, MDA, MPO, neuronal degeneration, vascular dilatation, inflammation, apoptotic appearance in the nucleus, loss of membrane and cristae in mitochondria, and dilatation in the endoplasmic reticulum were observed due to degeneration in the neuron structure. In the electron microscopic examination of the trauma + thymoquinone group, the membranes of the nuclei of the glial cells were thick and euchromatin, and mitochondria were shortened in length. In the SCI group, pyknosis and apoptotic changes were observed in neuronal structures and nuclei of glia cells in the substantia grisea and substantia alba region, along with positive Caspase-9 activity. An increase in Caspase-9 activity was observed in endothelial cells in blood vessels. In the SCI + thymoquinone group, Caspase-9 expression was positive in some of the cells in the ependymal canal while the cuboidal cells showed a negative Caspase-9 reaction in the majority. A few degenerated neurons in the substantia grisea region showed a positive reaction with Caspase-9. In SCI group, pSTAT-3 expression was positive in degenerated ependymal cells, neuronal structures, and glia cells. pSTAT-3 expression was positive in the endothelium and surrounding aggregated cells of the enlarged blood vessels. In the SCI+ thymoquinone group, pSTAT-3 expression was negative in most of the bipolar and multipolar neuron structures and glial cells in ependymal cells, enlarged blood vessel endothelial cells. CONCLUSIONS: It has been thought that thymoquinone application in spinal cord injuries may be an antioxidant that can be recommended as an alternative treatment in suppressing the apoptosis of neural cells by significantly reducing the inflammation process.

Endothelin 1, NF-κB, and ADAM-15 expression in diabetic foot wounds.

OBJECTIVES: The diabetic foot is an important and destructive complication of diabetes. This study examined 65 individuals (35 males, 30 females) diagnosed with diabetic foot with open wounds on their feet. METHODS: After washing the foot with isotonic solution, the wound was debrided and the excised tissues (diabetic dermis) were fixed with neutral buffered 10 % formalin solution. Specimens stained with haematoxylin-eosin, endothelin-1 (ET-1), nuclear factor kappa B (NF-κB), and ADAM 15 antibodies were used to examine angiogenesis, cytokine activity, and the extracellular matrix, respectively. RESULTS: Histopathologically, in the diabetic feet of males, leukocytes, lymphocytes, and macrophages were spread diffusely throughout the lesion, with inflammatory cells invading all layers of blood vessels. In the diabetic feet of females, dilation and congestion of the blood vessels, degenerative changes in the subendothelial layer, and perivascular infiltration by lymphocytes were observed. ET-1 was expressed in inflammatory cells around pre-capillary vessels in the stromal area. NF-κB was expressed in macrophages around blood vessels, and in nodular organised cells distributed throughout the perivascular space. ADAM 15 were expressed in fibroblasts, endothelial cells, and inflammatory cells. Blood parameters differed significantly between diabetic and non-diabetic patients (Significant at p < 0.005, p < 0.001 and p < 0.0001)Conclusion: ET-1 expression in the endothelial cells of diabetic foot ulcers is an important determinant of insulin resistance at the onset of disease and induces macrophages to produce NF-κB, which regulates inflammation. It is thought that ADAM 15 contributes to angiogenic effects as a means of stimulating endothelial cells (Tab. 2, Fig. 3, Ref. 31).

Histopathological changes in the choroid plexus after traumatic brain injury in the rats: a histologic and immunohistochemical study.

BACKGROUND: Traumatic brain injury (TBI) is in part associated with the disruption of the blood-brain barrier. In this study, we analysed the histopathological changes in E-cadherin and vascular endothelial growth factor (VEGF) expression after TBI in rats. MATERIALS AND METHODS: The rats were divided into two groups as the control and the trauma groups. Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight-height impact. After 5 days of TBI, blood samples were taken under ketamine hydroxide anaesthesia and biochemical analyses were performed. The control and trauma groups were compared in terms of biochemical values. RESULTS: There was no change in glutathione (GSH) levels and blood-brain barier permeability. However, malondialdehyde (MDA) and myeloperoxidase (MPO) activity levels increased in the trauma group. In the histopathological examination, choroid plexus in the lateral ventricle, near the pia mater membrane, was removed. In the traumatic group, some of epithelial cells were hyperplasic. Some of them were peeled off the apical surface and had local degeneration. CONCLUSIONS: In addition, we observed congestion in capillary vessels and mononuclear cell infiltration around the vessels. After TBI, the increase in VEGF levels, vascular permeability, and interaction with VEGF receptors in endothelial cells lead to oedema of the vessel wall. On the other hand, E-cadherin expression decreased in the tight-junction structures between epithelial cells and basal membrane, resulting in an increase in cerebrospinal fluid in the intervillous area.

Effects of nicotine administration in rats on MMP2 and VEGF levels in periodontal membrane.

BACKGROUND: Nicotine is associated with increased incidence of periodontal disease and poor response to therapy. This article aimed at identifying the expression of matrix metalloproteinases 2 (MMPs2) and vascular endothelial growth factor (VEGF) proteins on extracellular matrix, fibrous distribution and angiogenetic development in periodontitis caused by nicotine effects on periodontal membrane. MATERIALS AND METHODS: In this experimental study, rats were divided into nicotine and control groups. While the rats in the nicotine group (n = 6) were administered 2 mg/kg nicotine sulphate for 28 days, the animals in the control group (n = 6) were only administered 1.5 mL physiologic saline solution subcutaneously for 28 days. RESULTS: Histological sections were prepared and immunohistochemically stained for MMP2 and VEGF. The sections stained with Trichrome-Masson were observed under light microscope. VEGF and MMP2 immunoreactivity of periodontal gingiva and dentin was assessed by immunohistochemical staining. CONCLUSIONS: Nicotine reduces MMP production, disrupts collagen synthesis and causes periodontitis. We observed that nicotine increases periodontitis by disrupting periodontal membrane and prevents tooth to anchor in dental alveoli by disrupting epithelial structure.

Multiple variant type thalamic infarcts: pure and combined types.

BACKGROUND AND PURPOSE: Variant topographic patterns of thalamic infarction with distinct manifestations have been classified into three territories: anteromedian, central, and posterolateral. The purpose of this study was to determine clinical, etiological, and radiological features of multiple variant thalamic infarcts. METHODS: We reviewed 8400 patients with a first clinical stroke included in the Ege Stroke Registry between 2000 and 2013. Among 80 patients with an acute multiple thalamic infarcts confirmed by MRI, we selected all patients with lesions outside the classical territories and studied their clinical, etiological, and radiological features. RESULTS: Among 8400 patients with first-ever stroke in our registry, 21 patients (26% of all multiple thalamic infarcts) showed infarction outside the classical territories, allowing us to delineate three variant distributions; (i) unilateral multiple variant infarcts [seven patients (9%) in the anteromedian, central, and posterolateral territories] presented with predominantly decreased vigilance (66% with right lesions, 75% with left lesions), cognitive impairment including amnesia (71%), aphasia (57%) in left-sided or bilateral lesions, and executive dysfunction (43%). The most frequent stroke mechanism was cardioembolism (43%). (ii) Bilateral multiple variant infarcts [five patients (6%)], with lesions on the variant territories of the thalamus, resulting in a variety of neurological and neuropsychological signs, consciousness disturbances (80%), sensory-motor deficits (80%). Cardioembolism (60%) was the most frequent etiology. (iii) Combined multiple variant and classical infarcts [nine patients (11%)], characterized by hemihypesthesia (89%) as the most frequent manifestation, followed by hemiataxia (78%), and cognitive deficits. Cardioembolism (56%) and large-artery disease of the vertebrobasilar system (33%) were the main stroke mechanisms. CONCLUSIONS: We described multiple variant topographic patterns of thalamic infarction with distinct manifestations and etiologies. We thought that multiple variant infarcts are the result of variation in thalamic arterial supply or reflect a source of embolism.

Nasal obstruction in adults: how it affects psychological status?

OBJECTIVE: This study investigated the psychological status of patients with unilateral or bilateral complete nasal obstruction. METHOD: The study included 49 consecutive cases of unilateral or bilateral complete nasal obstruction. In order to assess participants' personality traits, both groups completed the Personality Belief Questionnaire, State-Trait Anxiety Inventory form, Beck Depression Inventory and Beck Anxiety Inventory. RESULTS: The groups were similar in terms of demographic characteristics. Patients with unilateral or bilateral complete nasal obstruction had higher scores on all the psychological assessments compared with the healthy controls, except for the Beck Anxiety Inventory. Although all personality assessment scores were higher in patients, the only differences that were statistically significant were in the dependent, antisocial and avoidant personality trait scores. CONCLUSION: The psychological conditions of patients with structural deformities that cause nasal obstruction may be affected, and appropriate treatment should be provided to improve their symptoms and quality of life.

Placental expression of vimentin, desmin and ultrastructural changes in the villi in patients with HELLP syndrome.

OBJECTIVES: To examine placental expression of vimentin and desmin in relation to ultrastructural changes within the placental villi in cases of HELLP syndrome. STUDY DESIGN: Formaldehyde-fixed and paraffin-embedded specimens of 15 healthy pregnant and 13 Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, placentas were used for Harris hematoxylin staining, vimentin and desmin immunohistochemistry, and transmission electron microscopy (TEM). RESULTS: Increased of fibrinoid necrosis in vascular wall and the periphery of villi were observed in sections of the placentas with HELLP syndrome. Increased expression of vimentin in the intravillous area and increased expression of desmin on blood vessel wall, were seen in placentas of patients with HELLP syndrome when compared to placentas of healthy pregnant. CONCLUSIONS: Augmentation of intermediate filaments, desmin, vimentin may disturb normal movements of endothelial cells, and may display placental dysfunction that is unable to compensate the endothelial instability and the related hypertension in HELLP syndrome. Further studies are needed to get more definit results and also to compare HELLP syndrome with preeclampsia.

CD34 expression of chorionic villous in pre-eclamptic placenta: an immunohistochemical and ultrastructural study.

In this study, pre-eclampsia, proteinuria, and edema associated with hypertension in pregnancy were assessed at the Dicle University School of Medicine Department of Obstetrics and Gynecology Clinic. One group included 20 pre-eclamptic pregnant women with gestational age 20-35 weeks of pregnancy and the same in the control group that included; however, 20 normotensive pregnant women. Histochemistry, immunohistochemistry, and electron microscopy techniques were used. Histopathological examination of syncytial nodes and stromal cells were observed in the increase in hyperplasia and hyalinization. The evaluation immunohistochemical of chorionic villi, placenta, and hematopoietic stem cell markers showed a positive reaction with CD34. Ultrastructural examination showed endoplasmic reticulum dilatation, degeneration of mitochondria in endothelial cells, and capillary vessel edema.

Gallic acid treatment protects intestinal tissue against ischaemia-reperfusion.

BACKGROUND: This study aimed to investigate the protective effects of gallic acid (GA) in the rat intestine against ischaemia-reperfusion (IR) injury. MATERIALS AND METHODS: Thirty male Wistar albino rats with a mean weight of 200-250 g were used. Animals were categorized into the sham, IR, and IR+GA groups. Ischaemia of the intestine was induced for 3 h by occluding the superior mesenteric artery (SMA) and then left for 3 h of reperfusion. In the IR+GA group, after ischaemia induction, 50 mg/kg GA was orally administered to the animals. Blood samples were collected for biochemical assays. Intestinal tissues were excised for histopathologic and immunohistochemical processing. RESULTS: Malondialdehyde (MDA) levels were increased, and catalase (CAT) and glutathione (GSH) levels were decreased in the IR group compared to the sham group. After GA treatment, MDA levels decreased and CAT and GSH levels increased in the GA-treated group compared to the IR group. In the sham group, normal intestinal histology was observed. In the IR group, the villi structures were completely degenerated. In the IR+GA group, histology was improved after GA treatment. In the sham group, the caspase-3 reaction was generally negative in the epithelium and glands. In the IR group, the caspase-3 reaction increased in apoptotic bodies and inflammatory cells. The caspase-3 reaction was negative in goblet cells and the epithelium. A moderate caspase-3 reaction was observed in the IR+GA group. The beclin-1 reaction was negative in epithelial cells and goblet cells in villi in the sham group. In the IR group, the beclin-1 reaction was positive in the degenerated villi. An intense beclin-1 reaction was also observed in some inflammatory cells. After GA treatment, the beclin-1 reaction was positive in a few cells. In general, moderate beclin-1 positivity was observed. CONCLUSIONS: Gallic acid, with its antioxidative effect, inhibited the apoptotic pathway (caspase-3) through beclin-1 regulation.

Angiotensin-1 and vimentin expression and ultrastructural examination in severe preeclampsia complicated by HELLP syndrome changes in the structure of the umbilical cord.

OBJECTIVE: The purpose of this study was to examine the histopathologic, ultrastructural and immunohistochemical changes in the umbilical cord in women diagnosed with HELLP syndrome. MATERIALS AND METHODS: Postpartum umbilical cords of 40 patients at the 35-38th week of pregnancy were included. 20 severe preeclamptic (HELLP) and 20 normal umbilical cords were used. After the follow-up of tissue parts of 10% formaldehyde solution for histopathology and immunohistochemistry, histopathological and angiopoietin-1 and vimentin antibodies were examined as immunohistochemical after routine paraffin follow-up. For electron microscope analysis, umbilical cord samples were taken into 2.5% glutaral aldehyde solution. RESULTS: In the statistical comparison, mean difference in increased diameter and additional anomaly on the ultrasound of preeclamptic patients was statistically different compared to control patients. In the HELLP group, hyperplasia and degenerative changes, pyknosis of the endothelial cell nuclei of the vessels and apoptotic changes in some regions were observed. Immunohistochemical analysis showed that endothelial cells, basal membrane and fibroblast cells in the HELLP group expressed high levels of vimentin. Angiotensin-1 expression was increased in amniotic epithelial cells, endothelial cells and some pericyte cells. CONCLUSIONS: As a result, it was observed that the signaling that started with trophoblastic invasion with the effect of hypoxia in severe preeclampsia and continued with dysfunction in endothelial cells was parallel to the increase in angiotensin and vimentin receptors. It is thought that the ultrastructural change in endothelial cells may cause disruption of the collagenized structure in Wharton gel, which supports this, and may cause adverse effects in fetal development and nutrition.

Weber's gland immune/histopathology in pediatric recurrent tonsillitis and obstructive tonsillar hypertrophy cases.

OBJECTIVE: Recurrent tonsillitis and obstructive tonsillar hypertrophy are very common in childhood and constitute the two major causes of tonsillectomy in this age group. There is no study in the literature on the immune/histopathological changes in the recurrent and obstructive tonsillar hypertrophy of Weber's glands. In this study, we aimed to histopathologically and immunohistochemically examine the Weber's glands of pediatric patients with recurrent. PATIENTS AND METHODS: A total of 63 patients, with 31 patients aged 6-9 who had surgery for recurrent tonsillitis, and 32 patients aged 6-11 years who had surgery for obstructive tonsillar hypertrophy, were included in the study. The removed Weber's glands were included in the obstructive tonsillar hypertrophy or recurrent tonsillitis group according to the patient's clinical diagnosis. All specimens were coded with a numbering method, where only the surgeon knew which patient was in which group. All specimens were evaluated in the same histology center and by the same histologist, unaware of the clinical diagnosis of the patients (blind). RESULTS: The comparison of Weber's gland immunohistochemical parameter scores of the groups revealed that the scores of the RT group were significantly higher for all three parameters (VEGF: t=6.777; p<0.001), (EGFR: t=4.386; p<0.001), (IL-6: t=5.072; p<0.001). The comparison of the groups in terms of inflammation, basement membrane thickening, myoepithelial cell and glycoprotein accumulation revealed significantly higher Weber's gland evaluation scores in the RT group for all four parameters. (inflammation: t=7.794; p<0.001), (basement membrane thickening: t=6.582; p<0.001), [myoepithelial cell: t=3.693; p<0.001), (glycoprotein accumulation: t=5.287; p<0.001)]. CONCLUSIONS: Histopathological and immunohistochemical examination of Weber's gland in pediatric recurrent tonsillitis and obstructive tonsillar hypertrophy cases revealed inflammatory changes in both disease groups. As expected, inflammatory manifestations were more common in the recurrent tonsillitis group. Besides, inflammatory changes detected in Weber's glands of obstructive tonsillar hypertrophy cases without a history of tonsillitis may contribute to the Weber's gland hypothesis, which attempts to explain the etiology of peritonsillar abscess.

Socio-demographic and clinical characteristics of individuals with diagnoses of eating disorder in a university hospital in Istanbul.

OBJECTIVE: This paper reports the first-ever description of a clinical eating disorder population from Turkey. The aim of this study was to examine the socio-demographic and clinical characteristics of individuals with diagnosis of eating disorders (IDED) referred to a university psychiatry clinic in Istanbul between 2003 and 2009. METHOD: The diagnoses and subtype of 111 IDEDs, the referral type to the hospital, setting of treatment, and state of involuntary hospitalization were evaluated by interview and semi-structured questionnaire. RESULTS: The clinical sample included 64 individuals with anorexia nervosa (AN), 38 with bulimia nervosa (BN), and 9 with eating disorder not otherwise specified (EDNOS), including only one male. Younger individuals and those with a lower BMI were significantly more likely to be family referred and hospitalized involuntarily. DISCUSSION: The overall socio-demographic features of the sample are generally consistent with data collected in other communities. However, aspects of the clinical features, referral types of eating disorders and subtypes exhibit some characteristics peculiar to our sample.

Effects of alloplastic graft material combined with a topical ozone application on calvarial bone defects in rats.

BACKGROUND: This study presents the evaluation of the damage in the bone tissue resulting from a calvarial defect in rats and the efficiency of exposure to an ozone application with an alloplastic bone graft on the calvarial bone damage. MATERIALS AND METHODS: Wistar male rats (n = 56) were divided into four groups: a control group (n = 14), defect and ozone group (n = 14), defect and graft group (n = 14), and defect, graft, and ozone group (n = 14). Under anaesthesia, a circular full-thickness bone defect was created in all groups, and the experimental groups were further divided into two sub-groups, with 7 rats in each group sacrificed at the end of the 4th and 8th weeks. Bone samples were dissected, fixed in 10% formalin solution, and decalcified with 5% ethylene-diamine-tetraacetic acid (EDTA). After the routine follow-up on tissues, immunostaining of osteopontin and osteonectin antibodies was applied to sections and observed under a light microscope. RESULTS: The control group exhibited osteopontin and osteonectin expression in fibroblasts and inflammatory cells at the end of the 4th week with an acceleration at the 8th week. Ozone administration elucidated new trabecular bone formation by increasing osteoblastic activity. Lastly, our observations underscore that a combination of allograft and ozone application increased the osteoblast, osteocyte, and bone matrix development at the 4th and 8th weeks. CONCLUSIONS: Exposure to an ozone application with an alloplastic bone graft on calvarial bone damage may induce osteoblastic activity, matrix development, mature bone cell formation, and new bone formation in rats.

Investigation of antioxidant effects of rosmarinic acid on liver, lung and kidney in rats: a biochemical and histopathological study.

BACKGROUND: The aim of the study was to investigate the protective effects of rosmarinic acid in rats exposed to hepatic ischaemia/reperfusion (I/R) injury. MATERIALS AND METHODS: Thirty-two rats were randomly classified into four groups of 8 rats each: laparotomy without medication, rosmarinic acid (dose of 50 mg/kg via oral gavage) followed by laparotomy, laparotomy followed by hepatic I/R, and hepatic I/R with rosmarinic acid. Serum aspartate aminotransferase, alanine aminotransferase, and malondialdehyde levels and total oxidant activity and total antioxidant capacity levels of the liver, lung, and kidney were assessed. The histopathologic assessment was also performed. RESULTS: Rosmarinic acid significantly reduced liver function test parameters and decreased oxidative stress and abnormal histopathologic findings in the liver. The oxidative stress in the lung significantly increased in the I/R group but significantly decreased in the I/R + rosmarinic acid group due to the addition of rosmarinic acid. Rosmarinic acid led to no reduction in oxidative stress in kidney following hepatic I/R injury. There were no statistically significant differences among the groups regarding histopathologic changes in kidney and lung sections. CONCLUSIONS: Rosmarinic acid has antioxidant properties and is an effective hepatoprotective agent. However, although rosmarinic acid provides useful effects in the lung by increasing antioxidant capacity and reducing oxidative stress after I/R injury, it does not ameliorate histopathologic changes. These findings suggest that rosmarinic acid is likely to provide favourable outcomes in the treatment of hepatic I/R injury.

Expression of vascular endothelial growth factor and glial fibrillary acidic protein in a rat model of traumatic brain injury treated with honokiol: a biochemical and immunohistochemical study.

BACKGROUND: Traumatic brain injury (TBI) leads to neuronal damage and neurological dysfunction. The aim of our study was to investigate the antioxidative effect of honokiol on TBI in rats with biochemical, histopathological and immunohistochemical methods. MATERIALS AND METHODS: Sprague-Dawley rats were subjected to TBI with a weight-drop device using 300 g/1 m weight/height impact. Forty-five rats were divided into three groups as control group, TBI group and TBI + honokiol group (5 mg/kg/day, i.p.). Honokiol (5 mg/kg) dissolved in dimethyl sulfoxide (DMSO) was intraperitoneally administered to rats for 7 days after the trauma. At the end of experiment, blood samples were taken from the animals and analysed with various biochemical markers. RESULTS: Histopathological examination of the trauma group revealed some degenerated pyramidal cells, dilatation and congestion in blood vessels, hyperplasia in endothelial cells, inflammatory cell infiltration around the vein and disruptions in glial extensions. In TBI + honokiol group, pyramidal neurons showed a decrease in degeneration, slight dilatation in blood vessels, improvement of endothelial cells towards the lumen, and reduction of inflammatory cells in the vessel. In TBI + honokiol group, vascular endothelial growth factor expression was positive in the endothelial and few inflammatory cells of the mildly dilated blood vessels. In the blood brain barrier deteriorated after trauma, it was observed that the glial foot processes were positive expression and extended to the endothelial cells in the TBI + honokiol group. CONCLUSIONS: Glial fibrillary acidic protein expression showed a positive reaction in these processes. Considering the important role of antioxidants and inflammatory responses in cerebral damage induced by traumatic head injury, honokiol is thought to be important in decreasing lipid peroxidation, protecting the membrane structure of blood brain barrier, degeneration of neurons and glial cells.

Evaluation of PECAM-1 and p38 MAPK expressions in cerebellum tissue of rats treated with caffeic acid phenethyl ester: a biochemical and immunohistochemical study.

BACKGROUND: This study aimed to investigate the antioxidative and anti-inflam- matory effects of caffeic acid phenethyl ester (CAPE) on damage caused to cere- bellum tissue by diffuse traumatic head trauma via biochemical, histopathologic, and immuno-histochemical methods. MATERIALS AND METHODS: Male Sprague-Dawley (300-350 g) rats were subjected to traumatic brain injury with a weight-drop device (300 g/1 m weight-height im- pact). Twenty-four adult rats were randomly divided into three equal groups of 8, including a control group, traumatic brain injury (TBI) group, and TBI + CAPE treatment group (10 µmoL/kg/i.p.). Cerebellum tissue samples taken from anterior lobe from all rats were taken 7 days after traumatic injury and were subjected to biochemical and histopathological analysis, as well as immunohistochemical ana- lysis for platelet endothelial cell adhesion molecule-1 (PECAM-1) and phosphate 38-mitogen-activated protein kinase (p38 MAPK). RESULTS: In the TBI group, the granular layer had dilatation and haemorrhage in the capillary vessels and inflammatory cell infiltration around the periphery of the blood vessels. In the TBI + CAPE group, the small capillaries in the white matter were slightly dilated, there were no inflammatory cells, and dense chromatin/ granular cells were observed in the granular layer. Also in the TBI + CAPE group, the Purkinje cells of the ganglion cell layer had ovoid nuclei, were chromatin- -rich, and their extensions protruded to the molecular layer. CAPE is thought to regulate inflammation, cell damage, and angiogenetic development by affecting the PECAM-1 and p38 MAPK proteins. CONCLUSIONS: These proteins are key modulators of endothelial integrity and neuroinflammation in vessels in response to endothelial damage as well as of the proinflammatory response in the cerebellum in response to traumatic damage.

Expression of matrix metalloproteinase-9 and tumour necrosis factor-alpha in the synovial cells of patients with meniscus tears.

BACKGROUND: A meniscus tear is a serious trauma that develops during swinging motion of the fixed foot. Meniscus tears may also be accompanied by divergence of the lateral ligaments of the knee joint. MATERIALS AND METHODS: We enrolled 45 males and 35 females with meniscal tears in the present study. Patients with local joint pain, swelling, difficulty climbing stairs, patellar creeping, difficulties with daily living activities, local pain on palpation, and walking and running complaints, were included. We performed preoperative magnetic resonance imaging. Synovial fluid (5 mL) was aspirated from the lateral suprapatellar pouch of each knee with meniscal pain with the patient in the supine position. Blood samples were taken and biochemical parameters were analysed. The Harris haematoxylin and eosin staining protocol was used to evaluate tissue samples, and the levels of anti-matrix metalloproteinase (MMP)-9 and anti-tumour necrosis factor alpha (TNF-α) antibodies were measured immunohistochemically. RESULTS: Increased numbers of lymphocytes and neutrophils, hyperplastic erythrocytes, and fibroblasts were observed in the joint fluid of females. In males, the fibroblast cells were hyperplastic and plasma cell numbers were increased. MMP-9 expression was elevated in plasma cells, fibroblasts, and neutrophils; and TNF-α expression was observed in lymphocytes and polymorphic nucleated cells. We suggest that increased fluid levels in inflamed joints with meniscal tears, and the associated inflammation, disrupt the cartilage matrix and elevate the production of cytokines such as TNF-α and MMP-9 via release from cells such as fibroblasts that synthesise these mediators. CONCLUSIONS: Anti-TNF-α treatment may prevent meniscal tears and prevent or slow the development of osteoarthritis.