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Background: This study was performed to investigate the light microscopic features of sustentacular cells in adrenal medulla in neonatal and adult male albino rats using an antibody against S-100 protein. S-100 expression in sustentacular cells is considered a reliable cell marker for this type of cells. Materials and methods: Twenty-four male albino rats were allocated into two groups, neonatal group (1 week old, 12 rats) and adult group (3 months old, 12 rats). Paraffin sections of the adrenal glands were immunostained for the expression of S-100 protein. Results: The results demonstrated differences in distribution, arrangement and structure of sustentacular cells in adrenal medulla in neonatal and adult rats. All sustentacular cells of adrenal medulla in all animals showed intense immunoreactivity for S-100 protein in their nuclei, perikarya, and cytoplasmic processes. Most of S-100 immunopositive sustentacular cells in adrenal medulla of neonatal rats are few, dispersed, small in size, and oval in shape with thin short bipolar cytoplasmic processes. These cells in adult rats are more numerous, larger in size, and stellate in shape with numerous slender, longer branched cytoplasmic processes. Conclusions: This study indicated that adrenal medullary sustentacular cells showed obvious morphological postnatal changes with aging suggesting structural and functional maturation. (Folia Morphol 2017; 76, 2: 246–251)
Background:The left ventricular hypertrophy (LVH) occurs in response to the haemodynamic overload in some physiological and pathological conditions. This study was designed to investigate the possible cardioprotective effect of simvastatin (SIM) treatment against isoproterenol (ISO)-induced LVH and the probable underlying mechanism in adult male Wistar rats. Materials and methods: Animals were allocated into four groups. Rats of control group received normal saline orally for 30 days and intraperitoneally for the last 7 days. Rats of SIM group received SIM orally (10 mg/kg/day in saline) for 30 days. Rats of ISO group received normal saline orally for 30 days and ISO intraperitoneally (5 mg/kg) for the last 7 days to induce LVH. Rats of ISO/SIM group received SIM for 30 days and ISO intraperitoneally for the last 7 days. At the end of the experiment, all animals were sacrificed by cervical decapitation under anaesthesia. Truncal blood was collected and serum was separated and used for biochemical assay. The heart was dissected and processed for histological and immunohistochemical studies. Results: The results of the present study confirmed the ISO-induced myocardial lesions including significant increase of heart weight (HW), heart weight/body weight (HW/BW) ratio, LVH, interstitial myocardial fibrosis (increased collagen types I and III), inflammatory cellular infiltration, necrosis of cardiomyocytes, and increased expression of inducible nitric oxide synthase (iNOS) and thioredoxin in cardiomyocytes. These changes were accompanied by significant increase in serum levels of troponin-T, creatine phosphokinase-MB (CPK-MB), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Co-administration of SIM to ISO-injected rats significantly reduced all these cardiac changes and serum biochemical markers in addition to marked depletion of iNOS and thioredoxin expression in cardiomyocytes. Conclusions: It is concluded that SIM co-administration attenuated ISO-induced cardiac lesions including LVH by inhibiting iNOS expression in cardiomyocytes. (Folia Morphol 2017; 76, 1: 15–27)
The objective of the present work was to study changes in collagen type I and type II distribution in the articular cartilage of immobilised and remobilised rabbit knee joints. Twenty-four adult male rabbits were divided into three groups. One of the groups was a control group with free movement. The right knee joints of animals of the other two groups were immobilised for 4 weeks, followed by a period of 10 weeks of remobilisation for animals of group 3. Collagen type I and type II in the articular cartilage of tibial medial condyle of the right knee joint were estimated immunohistochemically in all groups. A degenerative process was evident after 4 weeks of immobilisation of rabbit knee joint leading to a partial shift in the density of collagen composition from type II to type I. After a period of 10 weeks of remobilisation, regenerative processes, evidenced by a restoration of collagen type II to normal, proceeded on top of degenerative processes, evidenced by the significantly higher content of collagen type I compared with normal. The present study pointed to the importance of assessment of collagen distribution as a relevant indicator for the functional properties of articular cartilage in immobilised and remobilised joints. (Folia Morphol 2015; 74, 2: 169–175)
This study was performed to investigate the effect of curcumin on cardiac myosin- -induced autoimmune myocarditis in rats and the change in thioredoxin (TRX) immunoreactivity in cardiomyocytes following curcumin treatment. Twenty-four six-week-old male Wistar rats were randomly allocated into 4 groups of 6 rats each. Group I received neither curcumin nor myosin. Group II received an oral solution of 1 g/kg/day of curcumin daily, from day 1 to day 21. To induce myocarditis, animals of both group III and group IV were injected by 1 mg of porcine cardiac myosin on days 1 and 8. In addition, animals of group IV received an oral solution of 1 g/kg/day of curcumin daily, from day 1 to day 21. Serum levels of creatine phosphokinase, troponin-T, tumour necrosis factor-alpha and interleukin-6 were estimated. Hearts were processed for histopathological and immunohistochemical studies. Serum biomarkers levels were significantly increased in myocarditis group as compared to other groups. The intake of curcumin significantly reduced the deviation in these markers. Sections of the wall of the heart from myocarditis group were characterised by inflammatory cell infiltration. Most of cardiomyocytes showed pyknotic nuclei and increased sarcoplasmic eosinophilia with strong immunoreactivity for TRX. Sections from myocarditis-curcumin group showed normal architecture with moderate immunoreactivity for TRX. The present study demonstrated that curcumin ameliorates acute myocarditis in rats and encouraged the estimation of serum level of TRX as a relevant indicator for the evaluation of the progress of acute myocarditis. (Folia Morphol 2015; 74, 3: 318–324)
Background: Acetaminophen (APAP) hepatotoxicity is characterised by an extensive oxidative stress due to depletion of glutathione (GSH), which results in massive lipid peroxidation and subsequent liver injury. The current paradigm suggests that mitochondria are the main source of reactive oxygen species (ROS), which impair mitochondrial function and are responsible for cell signalling resulting in cell death. This study was designed to compare the potential impact of thymoquinone (THQ), and/or curcumin (CURC) on liver injury induced by APAP toxicity in rats. Materials and methods: Serum levels of alanine transaminase, aspartate transaminase, total bilirubin, and total protein were measured. In addition, liver nitric oxide (NO), malondialdehyde, reduced glutathione (GSH), and superoxide dismutase (SOD) were estimated. Moreover, these biochemical parameters were confirmed by histopathological and immunohistochemical investigations for the expression of thioredoxin, iNOS and caspase 3. Results: Acetaminophen toxicity elevated most of the above-mentioned parameters but decreased GSH, SOD, and total protein levels. Histologically, liver sections demonstrated liver injury characterised by hepatocellular necrosis with nuclear pyknosis, karyorrhexis and karyolysis. Immunohistochemical study revealed increased expression of iNOS and caspase 3 proteins, while the thioredoxin protein expression was decreased. Conclusions: Treatment with the THQ and CURC regulated the biochemical and histopathological alterations induced by APAP toxicity. It was concluded that the combination strategy of THQ and CURC might be considered as a potential antidote in combating liver injury induced by APAP with minimal side effects. (Folia Morphol 2019; 78, 4: 773–788)
Background: The outcome of the autograft therapy for Parkinson’s disease including autologous cells from adrenal medulla was disappointing. This could be attributed to the pathological process in Parkinson’s disease affecting cells of the adrenal medulla. This study was performed to investigate the histopathological changes in the adrenal medulla of AS/AGU rat, a model of Parkinson’s disease, in comparison with Albino Swiss (AS) rats. Materials and methods: A total of 24 male AS rats were divided into four groups, each of 6 animals: AS W1 — AS rats aged 1 week; AS adult — AS adult rats; AS/ /AGU W1 — AS/AGU rats aged 1 week; and AS/AGU adult — AS/AGU adult rats. The rats were sacrificed and the adrenal glands were dissected and processed for histological staining with haematoxylin and eosin and periodic acid Schiff and for immunohistochemical staining for S100 protein, ubiquitin and tyrosine hydroxylase. Results: The histological investigation of the adrenal medulla of AS/AGU rats showed vascular congestion, inflammatory cellular infiltration, pyknotic nuclei, necrotic chromaffin cells and medullary inclusion bodies. The immunohistochemical investigation of AS/AGU rats showed a statistically significant decrease in the expression of S100 protein, ubiquitin and tyrosine hydroxylase compared to AS rats. Conclusions: The histological and immunohistological changes in the adrenal medulla could explain the failure of outcome of adrenal autograft therapy in Parkinson’s disease. (Folia Morphol 2017; 76, 1: 28–37)
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