histological study on the effect of pentoxifylline on acute lung injury induced by renal ischemia reperfusion

Kidney ischemia-reperfusion injury [IRI] occurs under many clinical conditions. It leads to acute kidney injury, which may affect various remote but important organs such as the lung. The aim of the present study was to investigate the effect of renal IRI on the lung structure and evaluate the possible protective effect of pentoxifylline [PTX]. Fifteen adult male Wistar rats aged 8-10 weeks and weighing 150-200 g were used in this study. They were divided into the following groups: group I [the control group] was subjected to sham operation; group II [the IRI group] was subjected to renal ischemia by bilateral clamping of the renal pedicles for 45 min and then allowed 24 h of reperfusion. Group III [the PTX-treated group] was given two doses of PTX [40 mg/kg] intraperitoneally and subjected to an ischemia-reperfusion procedure as performed in group II. Lung specimens were processed for light and electron microscopic examination. The mean thickness of the interalveolar septa and the mean number of type-II pneumocytes were measured. Group II showed diffuse lung injury affecting mainly the alveoli, which appeared flooded with exudate and red blood cells, which also extravasated in the interstitium. There was vacuolation of the cytoplasm of both type-I and type-II pneumocytes with significant increase in the number of type-II cells and depletion of lamellar bodies. Significant increase in the mean thickness of the interalveolar septa was detected and it showed infiltration by macrophages and neutrophils. PTX caused marked improvement in the lung structure after ischemia-reperfusion. Most of the alveoli appeared empty and a few of them showed minimal red blood cells and macrophages. Thin interalveolar septa were detected with thickness comparable to that of the control group. Renal IRI caused alteration in the lung structure, which was ameliorated by PTX administration

Effect of alpha-lipoic acid on fundic gastric mucosal damage induced by acetyl salicylic acid: a histological study

alpha-Lipoic acid [ALA], an endogenous agent, has been shown to combat oxidative stress. The aim of the study was to evaluate the protective effect of ALA on fundic gastric mucosal damage induced by acetyl salicylic acid [ASA]. Fifty adult male albino rats were divided into four groups: group I [the control group], group II that received ALA for 2 weeks [subgroup IIa] and for 4 weeks [subgroup IIb], group III that received ASA for 2 weeks [subgroup IIIa] and for 4 weeks [subgroup IIIb], and group IV that received ALA 30 min before ASA for 2 weeks [subgroup IVa] and for 4 weeks [subgroup IVb]. At the end of the experiment, specimens from the fundus of the stomach were processed for light and electron microscopic examinations. The mean number of proliferating cell nuclear antigen [PCNA]-positive cells, parietal cells, and the mean thickness of the fundic mucosa were measured and the results were statistically analyzed. Examination of sections revealed that ASA for 2 weeks induced widening of the gastric pits and focal mononuclear cellular infiltration. The mucous content of the mucosa was apparently increased and PCNA-positive cells were significantly decreased compared with the control group. ASA for 4 weeks resulted in extensive desquamation, thinning out of the mucosa, and diffuse mononuclear cellular infiltration. The collagen content of the lamina propria showed an apparent increase, whereas the mucous content showed an apparent decrease. The parietal cell count and the PCNA-positive cells were significantly decreased compared with the control group. In ultrathin sections, parietal cells showed cytoplasmic vacuoles, decreased intracellular canaliculi, and mitochondria, whereas the chief cells showed dilated rough endoplasmic reticulum and decreased secretory granules. Concomitant use of ALA showed a histological profile nearly comparable with that of the control group in both subgroups IVa and IVb. ALA administration prevented the structural changes of the gastric mucosa induced by ASA

Effect of zinc-free diet from weaning through puberty on the structure of the testis in albino rats, with a special focus on the Leydig cells

Zinc is an essential trace element. Many physiological processes would be impaired if zinc is not supplied in sufficient quantities in the diet. The aim of the work was to evaluate the effect of a zinc-free diet from weaning through puberty on the testicular structure of rats, with a special focus on the Leydig cells. Twenty weaned rats were divided into three groups. Group I [the control group] was fed a balanced diet. Group II [the zinc-free group] was fed a zinc-free diet for 3 months. Group III [the recovery group] was fed a zinc-free diet for 3 months, followed by a balanced diet for 1 month. At the end of the experiment, rats were weighed and blood samples were collected to measure the level of serum testosterone hormone. The testes were removed, weighed, and processed for light and transmission electron microscopic study. The zinc-free group showed a significant decrease in the mean body weight, testis weight, and serum testosterone level compared with the control group. The light and electron microscopic examination showed loss of most of the spermatogenic cells accompanied by variable degrees of degeneration in the form of karryorhexis and haphazard chromatin content. In the interstitial tissue, there was accumulation of exudate. Many Leydig cells showed dilated smooth endoplasmic reticulum and mitochondria. Others cells showed accumulation of glycogen. Most of these changes were reversed after receiving the balanced diet in the recovery group. A zinc-free diet altered the structure of both the seminiferous tubules and the Leydig cells. Most of these alterations were reversed by zinc replenishment. Zinc is considered an essential element for maintaining testicular structure and spermatogenesis process

Arsenic-induced toxicity in the endometrium of adult albino rat and the possible role of human chorionic gonadotropin hormone: a histological study

Arsenic is a toxic mutagenic metalloid and a major pollutant of water. Exposure to arsenic produces various adverse reproductive effects. Human chorionic gonadotropin [hCG] has an important role in the female reproductive system. The aim of the study was to investigate the effects of sodium arsenite on the structure of the endometrium of adult rats and evaluate the possible role of hCG in the amelioration of these changes. Thirty-six adult female rats were used in this study. They were divided into three equal groups: group I [the control group]; group II, in which the animals received sodium arsenite orally for 28 days; and group III, in which the animals were subcutaneously injected with hCG for 28 days, together with the previous dose of sodium arsenite. Specimens of the endometrium were taken at diestrous phase and prepared for light and scanning electron microscopic examinations. Moreover, morphometric measurements were taken to measure the height of the surface epithelium and the diameter and number of endometrial glands, and the results were statistically analyzed. Arsenite treatment prolonged the diestrous phase. The surface epithelium showed a significant reduction in height as compared with the control group and some parts showed focal degeneration and shedding. The endometrial stroma showed irregularly shaped cells and an apparent increase in collagen fibers. Small and atrophied glands were seen. Scanning electron microscopic examination revealed a decrease in the number of cells with pinopodes and a decrease in the number of pits of glands. Concomitant administration of arsenite and hCG resulted in regular estrous cycles. The structure of the endometrium was improved as compared with that of the arsenic-treated group. Sodium arsenite altered the structure of the endometrium and the phases of the estrous cycle. Concomitant administration of hCG with arsenic improved the structure of the endometrium and the regularity of the estrous cycle

Role of thyroxin versus Brewer's yeast supplementation in amelioration of pancreatic alterations induced by hypothyroidism in adult male albino rats

Induction of hypothyroidism by carbimazole could affect many glands including the pancreas. Brewer's yeast, a herbal product, is recently under research for its possible uses. The aim of the study was to study the microscopic, morphometric, and biochemical changes in the pancreas of hypothyroid rats and to evaluate the role of thyroxin versus Brewer's yeast in amelioration of these changes. Sixty adult male albino rats were randomly divided into five groups. Group I rats served as a control group. Group II rats received carbimazole. Group III rats received carbimazole followed by thyroxin. Group IV rats received carbimazole followed by Brewer's yeast. Group V rats received only Brewer's yeast. At the end of the experimental period, specimens from the pancreas were processed for light and transmission electron microscopic examinations and immunostaining for Ki-67. Biochemical analysis for T3, T4, and insulin was performed. In addition, body mass gain and pancreatic mass were measured. All parameters were statistically analyzed. Group II specimens revealed congestion of blood vessels and cellular infiltration. Acinar cells showed pyknotic nuclei, hyalinization, and vacuolation of the cytoplasm, with few zymogen granules. beta Cells of the islets of Langerhans revealed depletion of organelles and small granules without their characteristic halo. Immunostaining revealed significant decrease in the percentage of Ki-67-positive nuclei. In group III, the acini revealed numerous secretory granules, few vacuoles, and euchromatic nuclei. beta Cells showed secretory granules with the characteristic halo. Group IV revealed less improvement in the histopathological changes as compared with group III. T3, T4, and insulin levels were significantly lower in hypothyroid rats in comparison with the control group, whereas administration of thyroxin showed restoration of these levels to near control values. Hypothyroidism showed a deleterious effect on the histological structure of rat's pancreas. Administration of thyroxin minimized these effects more than administration of Brewer's yeast

Cardiac effects of bee venom in rats

To elucidate the possible effects of bee venom [BV] on cardiac electrophysiological properties in vivo, the inotropic and chronotropic properties of the isolated hearts in vitro, and the cardiac responsiveness to progressive adrenergic stimulation by isoproterenol. This randomized control study was conducted in the Physiology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt, from April to June 2010. This work was carried out on 22 female Wistar rats. Rats were allocated into 2 groups; BV-treated group [rats were treated with BV in a dose of 20 micro g/kg body weight, administered subcutaneously for 4 days], and the control group. Prior to sacrifice, the studied animals underwent electrocardiographic [ECG] assessments under anesthesia. Thereafter, isolated hearts were studied in a Langendorff preparation for their intrinsic properties, and their responses to beta-adrenergic stimulation. Following recovery, heart tissues were used for assessment of myocardial calcium content, and for histological examination. No abnormal ECG findings were observed in the BV-treated group. The BV treatment enhanced tension generation in the cardiac muscle in response to beta-adrenergic stimulation, and improved the inotropic cardiac reserve. Calcium content of the myocardial tissue of BV-treated group was significantly increased. Histological examination of the cardiac tissue of BV-treated group demonstrated preserved myofilament and mitochondrial ultrastructural integrity. The BV enhanced the cardiac inotropic reserve to beta-receptor agonists. Meanwhile, BV protected the heart against calcium overload-induced injury

Protective effects of vitamin E against myocardial ischemia/reperfusion injury in rats

To clarify the cardioprotective effects of a short course of vitamin E treatment [vit E] as compared with a nitric oxide donor, nitroglycerin [GTN] against ischemia-reperfusion induced heart injury in rats. This randomized control study was conducted in the Physiology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt from 1st June to 31 August 2009. This work was undertaken on 28 female Wistar rats weighing 150-200 gin. Rats were allocated into 4 groups; control group [non-treated], GTN-treated group [rats received GTN intraperitoneally 25 minutes before sacrifice, in a dose of 120 microg/kg body weight], vit E-treated group [rat received vit E by oral tubal feeding 16-20 hours before sacrifice, in a dose of 250 mg/rat], and vit E and GTN-treated group [rats received vit E and GTN as in both GTN-treated group and vit E-treated group]. After sacrifice, the hearts were excised and perfused in a Langendorff preparation and subjected to 30 minutes global ischemia and reperfused for 30 minutes, Following reperfusion, heart tissues were used for assessment of malondialdehyde [MDA] and nicotinamide adenine dinucleotide [NAD][+], and for histological examination. Vitamin E treatment resulted in an enhanced post-ischemic recovery of systolic function in vit E-treated groups [vit E-treated group, and vit E and GTN-treated group] compared to the control group. Post-ischemic recovery of coronary flow was enhanced in the vit E-treated group compared to the GTN-treated group. Post ischemic tissue degeneration indicators: MDA, and NAD[+] indicated a cardioprotective effect of vit E. Histological study revealed marked improvement of myocytes and mitochondrial structure in the vit E-treated group as compared with the control group. Preconditioning with vit E treatment afforded substantial recovery of post-ischemic contractile, and vascular functions compared to GTN treatment, the mechanism might involve less opening of mitochondrial permeability transition during postischemic reperfusion

Effect of medical ozone therapy on diabetes-induced cardiac dysfunction

Diabetic metabolic dysregulation is accompanied by oxidative stress that could possibly lead to dysfunction in cardiac myocytes. The aim of this study was to elucidate the effect of controlled medical ozone therapy to diabetic rats on ischemia reperfusion insult in isolated rat hearts. Both long-term [12 weeks duration] and short-term [20 days duration] treatment were investigated. Rats of each duration were divided into non-diabetic control group and streptozotocin-induced diabetic group, the latter group being further divided into two subgroups, namely, a group receiving medical ozone and the other remaining untreated. Long-term groups were studied for the cardiac responses before and after ischemia reperfusion. Short-term groups were used to assess the degree of leukocytic adhesion to coronary endothelium. In both durations, serum levels of CPK and TNF-alpha were determined. Long-term ozone therapy to diabetic rats improved myocardial depression before and after ischemia reperfusion, with reduction in ischemia reperfusion injury. Short-term therapy resulted in an attenuating effect on leukocyte adherence to coronary vascular endothelial cells after ischemia-reperfusion. The present data show the cardioprotective effect of medical ozone therapy on ischemia reperfusion injury in diabetic rats. The reduction in TNF-alpha may represent a mechanism for such protection. Prohibiting leukocyte-endothelial adhesion and transmigration may be useful in decreasing leukocyte-dependent post-reperfusion injury