histological changes in the adult rat cerebral cortex after transient cerebral ischemia and the neuroprotective effect of erythropoietin

The field of cerebral ischemia has attracted many investigators due to its multiple etiological factors as well as its early and late consequences. The objective of this study was to clarify the hiistopathological changes in the adult rat cerebral cortical neurons after transient cerebral ischemia and to evaluate the neuroprotective effect of erythropoietin. Transient ischemia was conducted by bilateral ligation of the common carotid arteries for five minutes and a group of rats were intraperitoneally injected with erythropoietin at the time of ligation. Twenty four hours after the operation many pyramidal nerurons were replaced by apoptotic bodies. The cells were shrunken, the nuclei were irregular and the chromatin was condensed. Moreover, other neurons showed degenerative change in each cytoplasmic organelle i.e. both apoptosis and necrosis were detected in the rat cerebral cortical neurons after transient ischemia. Twenty eight days after the operation, signs of neuronal degeneration like apoptosis and some features of necrosis were still observed. Conversely the pictzure differed completely in erythropoietin treated animals. There were very few apoptotic bodies and the neurons attained normal shape of their cell body, dendrites and axons. The cytoplasmic organelles appeared nearly normal. It could be concluded that injection of erythropoietin could enhance recovery of the ischemic neurons and therefore, an excellent clinical outcome will be achieved in patient suffering from cerebral stroke

Streptozotocin-induced diabetic cystopathy in albino rat. An ultrastructural and immunohistochemical study

It was suggested that urinary bladder dysfunction can be considered as one of the most common complications of diabetes. Therefore, this study was designed to clarify the ultrastructural changes in the smooth muscles of the urinary bladder in diabetic rats and to ascertain the role of iNOS, in an attempt to investigate the possible mechanism of these histopathological changes. Thirty adult male albino rats were used in this study. The animals were divided into three equal groups; A served as sham-injected control, while the animals of group B were intraperitoneally injected with a single dose of streptozotocin [50 mg/kg body weight/ rat] and left under observation tor 8 weeks. The rats of group C were intraperitoneally-injected with the same dose of streptozotocin and left for 18 weeks. Specimens from the urinary of the animals of all groups were to obtain paraffin blocks which were cut and immunohistochamically stained for demonstration of iNOS activity. In addition, small specimens were processed and prepared for electron microscopic study. The smooth muscles cells showed progressive ultrastructural changes in the form of degenerated mitochondria, apparent increase in of the pinocytotic vesicles which were relatively electron lucent and degenerated in the cytoplasm that were devoid of actin and myosin filaments, in addition, corrugated cell membranes and widened gap junctions were observed. These myocytes showed strong positive reactions for iNOS as compared with the control group. The connective tissue stroma between adjacent cells showed degenerated nerve fibres forming myelin body-like structures, activated fibro-blasts with dilated endoplasmic reticulum cisternae and increased collagen deposition. These changes were more marked in the animals of the third group. Therefore, urinary bladder biopsy may be of value in early diagnosis of diabetic cystopathy with a more positive impact on management. Moreover, the increased iNOS expression can be considered as an indicator of oxidative stress and thus the use of antioxidants might have a role in better management of such condition

Microscopic changes in the myocardium of streptozotocin-induced diabetic rats and the effect of vitamin C administration

Diabetic cardiomyopathy can be considered as one of the most common complications of diabetes. Oxidative stress and the production of reactive oxygen species [ROS] were considered to play a key role in the pathogenesis of this cardiomyopathy. Accordingly, this study was planned to detect the biochemical disorders and structural changes in the cardiac muscle in experimentally-induced diabetic rats and to emphasize the role of vitamin C, which could be considered to have an antioxidant effect, in the correction of these abnormalities. Thirty adult male albino rats were classified into three equal groups; group A served as Sham-injected control, while group B rats were turned diabetic by a single intraperitoneal injection of streptozotocin in a dose of 50 mg / kg body weight / rat and left under observation for 16 weeks. The animals of group C were turned diabetic by the same method, but they received vitamin C by stomach tubes for one week before and 16 weeks after induction of diabetes in a single daily dose of 200 mg /kg body weight / rat. Biochemically, significant hyperglycemia and an increase in serum malondialdehyde [MDA] levels with a significant decrease in myocardial glutathione [GSH] were noticed in the animals of group 6 [16 weeks after induction of diabetes]. This was accompanied with extensive microscopic changes in the cardiac muscle in the form of depletion of glycogen content, increased collagen deposition and decreased ATPase activity. Ultrastructurally, myofibrillar disarray in the form of discontinuous, irregular and fragmented Z lines, loss of microfilaments and disorganization of sarcomeres was noticed. The mitochondria appeared irregular in shape with heterogeneous electron dense matrix and disrupted or absent cristae. In addition, appearance of secondary lysosomes and absence of glycogen granules were encountered. The intercalated discs showed a large area having no cellular junctions. These biochemical and morphological abnormalities were apparently reduced in the diabetic rats that received vitamin C. Accordingly, the daily use of vitamin C might play an essential role in the protection against diabetes-induced cardiomyopathy with a more positive impact on management

Ultrastructural and immunohistochemical study of ITO cells of rat in carbon tetrachloride -induced liver fibrosis and the protective effect of vitamin A

The hepatic stellate cells, Ito cells, were known to play multiple roles in liver histopathology. This study was undertaken to explore the role of these cells in carbon tetrachloride [CCL4]- induced liver fibrosis, histologically and immunohistochemically, and to investigate the protective effect of vitamin A. Fifty rats were used and divided into three groups. The first group served as a control. The rats of the second group were injected twice a week with CCL4 for eight weeks, while the animals of the third group were pretreated with Vitamin A before injection of CCL4. At the end of each experiment, specimens from the liver of the animals were taken and processed for transmission EM study and immunohistochemical demonstration of GGaI fibrillary acidic protein [GFAP] and alpha smooth muscle actin [alphaSMA]. Eight weeks after CCL4 administration, thick and irregular C.T. septa with formation of definite lobules and pseudolobules were detected. GFAP-positive to cells were few in number intralobularly and in the C. T. septa. In contrast, there were numerous alphaSMA-positive cells. However, in Vitamin A-pretreated rats numerous GFAP-positive ito cells and few alphaSMA-positive cells were detected in-side the lobules. Ultrastructurally, three types of Ito cells were detected in the liver of CCL4-intoxicated rats. Some Ito cells resembled myofibroblasts, others contained many lipid droplets and activated rER, while septal Ito cells attained a fibroblast like feature. On the contrary, in Vitamin A pretreated group, Ito cells contained numerous lipid droplets and had few dilated rER cisternae. From this current study, we that immunohistochemical demonstration of GFAP and alphaSMA may be alpha method for studying hepatic fibrogenesis. Moreover, it is recommended that, Vitamin A may have a protective effect against carbon tetrachloride-induced hepatotoxicity