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1.
Egyptian Journal of Histology [The]. 2014; 37 (2): 360-372
in English | IMEMR | ID: emr-160214

ABSTRACT

Impairment of wound healing in diabetic patients is an important clinical problem. Various studies have suggested that using regenerative medical therapy could be a good solution. Mesenchymal stem cells are nonhematopoietic progenitor cells that have high differentiation potential and could be isolated from bone marrow and other tissues. The aim of this study was to assess the role of stem cells in the healing of diabetic skin wounds of male albino rats. Forty-two male albino rats were used in this study. Seven of them of an average weight of 50-70 g were used for extraction of bone marrow. The rest of the rats were of an average weight of 150-200 g and were used as animal models. The animals were divided into four groups: group I, comprising rats from which the bone marrow was extracted; group II, which formed the control group; group III, comprising diabetic wounded rats; and group IV, in which wounded diabetic rats were treated with bone marrow-derived mesenchymal stem cells. Diabetes was induced in rats by means of a single intraperitoneal injection of streptozotocin. Wounds of groups III and IV were examined after 3 and 7 days. Skin specimens were processed and stained with H and E and Masson's trichrome. Re-epithelization with complete closure of the wound was noted in the stem cell-treated group after 7 days. There was a significant increase in the number of hair follicles/high-power field and increase in the collagen content of the dermis in the stem cell-treated groups compared with the untreated groups. Bone marrow-derived mesenchymal stem cells can be effectively used in the treatment of diabetic wounds


Subject(s)
Male , Animals, Laboratory , Mesenchymal Stem Cells/physiology , Diabetes Mellitus, Experimental/complications , Wounds and Injuries/therapy , Microscopy, Polarization/statistics & numerical data , Treatment Outcome , Rats
2.
Egyptian Journal of Histology [The]. 2014; 37 (3): 592-602
in English | IMEMR | ID: emr-160235

ABSTRACT

Changes in lifestyle and food habits increase the prevalence of nonalcoholic fatty liver disease [NAFLD]. It is a chronic condition that has no or few symptoms. It may be accompanied by inflammation and insulin resistance. Moreover, it is closely linked to diabetes. Metformin is an antidiabetic agent that can improve insulin resistance. The study was conducted to investigate the effect of metformin on liver injury induced by a high-fat diet. The study lasted for 12 weeks. Thirty-six adult male albino rats were used and divided into four groups. Group I was the control group. Group II rats received metformin. Group III rats were fed a high-fat diet for induction of NAFLD. Group IV rats were fed a high-fat diet for induction of NAFLD and then administered metformin orally in the last 4 weeks of the study. Liver specimens were processed for light and electron microscopic examination. Moreover, liver weight index was determined, and biochemical, morphometric, and statistical studies were performed. Induction of NAFLD [group III] resulted in severe insulin resistance. Hepatocytes showed macrovesicular and microvesicular steatosis, ballooning, and lobular inflammation. The number of positive cells and the reaction for tumor necrosis factor-alpha in group III apparently increased as compared with group IV. Lipid droplets, loss of mitochondrial cristae, and dispersion of rER were detected in group III. Metformin improved insulin resistance, and liver histological changes were fewer than those in group III. Metformin can greatly improve liver histological changes associated with a model of NAFLD


Subject(s)
Male , Animals, Laboratory , Metformin , Non-alcoholic Fatty Liver Disease/therapy , Immunohistochemistry/statistics & numerical data , Microscopy, Electron/statistics & numerical data , Rats
3.
Egyptian Journal of Histology [The]. 2010; 33 (1): 55-67
in English | IMEMR | ID: emr-136375

ABSTRACT

Restoration of the blood flow and reintroduction of oxygen after deprivation accelerate tissue injury. The insult of intestinal ischemia reperfusion [PR] is not necessarily limited to the intestine itself, but involves the severe destruction of the other tissues because of the reperfused oxygenated blood. Many reports indicated that I/R is an important inciting event in the pathogenesis of multiple organ system failure, which is the leading cause of death in critically ill patients. So, the aim of this study was to evaluate the possible protective role of pyrrolidine dithiocarbamate [PDTC] on liver and small intestinal injury following mesenteric ischemia reperfusion. The study was performed on forty adult male albino rats weighting 200-250 gm that were divided into three groups. Group I: Control animals which divided into untreated and sham operated [10 animals each]. Group II: Intestinal ischemia reperfusion animals, which were underwent one hour ischemia and two hours reperfusion. Group Ill: Animals received 200 mg/kg PDTC intraperitoneally one hour before intestinal ischemia reperfusion procedure. Parts were taken from the liver and jejunum were processed for histological examination and other jejunal parts for scanning electron microscopic examinations [SEM]. Immunohistochemical expression of NF-ka B factor in the liver was investigated. A variety of changes were observed in the jejunal ranging from epithelial separation and loss of the brush border to cellular lysis, destruction of villi, cellular infiltrations, hemorrhages and basal glandular ulcerations. The liver showed areas of edema fluid, hemorrhages, mononuclear cellular infiltration and increased expression of INF-ka B factor. Treatment with PDTC resulted in improvement in most of the histological changes induced by intestinal ischemia-reperfusion in the jejunum and liver. Therefore, PDTC can be considered as an effective protecting agent during intestinal ischemia reperfusion and can be used clinically in such instances

4.
Egyptian Journal of Histology [The]. 2009; 32 (2): 315-323
in English | IMEMR | ID: emr-136358

ABSTRACT

Cataract formation is one of the irreversible processes for which modem medical science has no definite cure except surgery. Drugs that may have prophylactic or curative effects for cataract are lacking. Naphthalene has wide industrial and commercial applications and it is well known that ingestion of naphthalene causes cataract in human and experimental animals. Curcumin, a widely used spice, has been proved to have an antioxidant activity in vitro and in vivo. The purpose of this study was to test the possible efficacy of curcumin in preventing cataract formation in a rat model. So, forty adult male albino rats weighting 100-120 gm were used in this study. They were divided into the experimental groups. Group I: Control animals. Group II: Animals received a dose of 0.7 g/kg of naphthalene solution orally daily for 90 days. Group III: Animals concomitantly administered curcumin with naphthalene in a dose of 75 mg/kg orally daily for the same duration. Slit lamp examination and retroillumination photography were done to all animals at the end of the experiment, then the rats were sacrificed and the lenses were removed and processed for histological and scanning electron microscopic [SEM] examination. Animals received naphthalene showed, by slit lamp photography, equatorial vacuoles and anterior subcapsular white opacities. Histologically, lens capsule was thin with hyperplasia of the lens epithelium. PAS stained deposits were also seen under the capsule with increased spacing between the lens fibers. Furthermore, the hexagonal cross sectional structure of lens fibers was lost in some areas. SEM showed loss of ball and socket interlocking between the lens fibers. Concomitant administration of curcumin with naphthalene resulted in amelioration of most of the histological changes induced by naphthalene. Therefore, curcumin may have a beneficial effect in protection against cataractogenesis

5.
Egyptian Journal of Histology [The]. 2007; 30 (1): 105-114
in English | IMEMR | ID: emr-82310

ABSTRACT

Type II diabetes is one of the most common chronic health problems characterized by insulin resistance. Unfortunately, this resistance is increasing at a very rapid rate due to changing lifestyles. Physical exercise could potentially contribute to prevention or delay of type II diabetes complications. This study focused on role of exercise in controlling skeletal muscle fibers changes due to type II diabetes. Forty adult male albino rats were used and divided into two groups: Group I [control group] included Ia and lb subgroups. Group II [diabetic group] included IIa, IIb subgroups. Type II diabetes was induced in group II by intake of 50% fructose solution for 8 weeks. In subgroups Ib and IIb, rats underwent an exercise swimming program for 4 weeks. In subgroup IIa, blood glucose level was elevated. Some muscle fibers appeared degenerated with homogeneous sarcoplasm and loss of striations. The mitochondrial content was decreased. With electron microscopy, mitochondria appeared pleomorphic and myofilaments were disrupted. In subgroup IIb, exercise greatly attenuated the histological changes seen in subgroup IIa. The skeletal muscle fibers had more or less similar appearance to control group. This work proved that exercise has a great role in controlling skeletal muscle structural changes due to type II diabetes


Subject(s)
Male , Animals, Laboratory , Muscle, Skeletal/pathology , Exercise , Muscle, Skeletal/ultrastructure , Microscopy, Electron , Rats , Models, Animal
6.
Egyptian Journal of Histology [The]. 2007; 30 (2): 301-310
in English | IMEMR | ID: emr-172509

ABSTRACT

Hippocampus is a vulnerable brain structure susceptible to neuronal atrophy following oxidative stress. Increased oxidative stress is an underlying cause of neuronal damage induced by ischemia /reperfusion [1 / R]. Oxygen free radicals are considered to be an important component involved in the pathophysiological tissue alterations in ischemia /reperfusion [1/ R] following oxidative stress. The present study was carried to investigate for any protective role of curcumnin and simvastatin on the structure of hippocampus of male albino rats exposed to ischemia. Fifty two adult male albino rats were used and divided into 6 groups. Group I [control group.], group II [sham-operated group,] group III [ischemic induced group] ,group IV[received curcumnin for 4veeks before induction of ischemia] ,group V [received simvastatin for 4weeks before induction of ischemia] group VI [received both curcumin and simvastatin for 4weeks before induction of ischemia]. The animals were sacrificed after 4 days of induction of ischemia. In group III, I /R led to degeneration of many pyramidal cells in area 1 of Corn Amninonis [CA1 area of hippocampus], apparent increase of astrocytes and a decrease of Nissl granules content. Group IV showed mild attenuation of generative changes seen in group III whereas astrocytes were still apparently increased. In group V, a greater cyroprolective effect was observed with simvastatin than curcumin. Many pyramidal cells appeared similar to control group, mild increase of Nissl granules content and an apparent slight increase of astrocytes were observed in group VI ,the pyramidal cells amid astrocytes had more or less similar appearance to control group. The present study showed a great protective effect for simvastatin on structure of hippocampus subjected to transient ischemia. This protective effect could be augmented by receiving curcumnin with simvastatin


Subject(s)
Male , Animals, Laboratory , Hippocampus/pathology , Protective Agents , Curcumin , Simvastatin , Treatment Outcome , Histology , Rats , Male , Adult
7.
Egyptian Journal of Histology [The]. 2005; 28 (2): 191-198
in English | IMEMR | ID: emr-70388

ABSTRACT

With the onset of menopause, reduced estrogen levels and insufficient calcium in diet create serious problems with resultant osteoporosis and fractures. Recent moves away from hormone replacement therapy suggested calcium, as the simplest and cheapest strategies to treat and prevent osteoporosis. Accordingly, this study was carried out to focus histologically on the efficacy of calcium in the treatment and prevention of osteoporotic bone loss in ovariectomized rats. Forty adult female albino rats weighing 200 gm were used and divided into four groups. Group I [control group] included non-ovariectomized untreated rats. Group II rats were ovariectomized on day 1 of the experiment and sacrificed on day 30 after ovariectomy. Group III rats were ovariectomized on day 1 of the experiment and received 27 mg calcium carbonate daily from day 30 to day 60 and then sacrificed. Group IV rats received the same dose of calcium carbonate daily for 30 days prior to ovariectomy and for 30 days after it. The rats were ovariectomized on day 30. Group II animals showed marked decrease in the cortical bone thickness and bone trabeculae were thin and discrete. In group III animals, the decrease in cortical and trabecular bone thickness was mild. Regarding group IV, the bone architecture was maintained so that the cortical bone, and the bone trabeculae were more or less comparable to the control group. From the results of this work, it is concluded that calcium supplementation was effective in reduction and prevention of osteoporosis in ovariectomized rats


Subject(s)
Female , Animals, Laboratory , Ovariectomy , Calcium Carbonate , Tibia , Histology , Rats , Models, Animal , Calcium
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