Histopathological Alterations In Lung Research Articles

Extra Virgin Olive Oil Nanoemulsion Attenuated Inflammatory Response in Lipopolysaccharide-Induced Sepsis

The provision of nutritional components in critical illness such as sepsis remains a big issue in clinical application, particularly through oral route due to intestinal integrity damaged-associated absorption problem. The aim of this research was to develop Extra Virgin Olive Oil (EVOO) nanoemulsion as a nutrient carrier to improve its permeability while maintaining the intestinal mucosa integrity in mouse model of lipopolysaccharide-induced sepsis. EVOO nanoemulsion was prepared by using ultrasonication-mild agitation method. EVOO nanoemulsion (1.5 mL) was administered to the mice through orogastric tube. The effect of EVOO nanoemulsion was evaluated by assessing the histopathological alterations in lung, measuring the activation of NFκB-p65 by immunohistochemistry of lung tissue, the levels of circulating Surfactant Protein-D (SP-D), tumor necrosis factor-alpha, interleukin (IL)-8, and IL-10. The main result, EVOO nanoemulsion decreased circulating SP-D level after 24 h. In conclusion, EVOO nanoemulsion is a promising carrier to improve nutrition absorption and decrease circulating SP-D as organ injury biomarker.

Ameliorative effect of N-acetyl cysteine on alpha-cypermethrin-induced pulmonary toxicity in male rats

Alpha-cypermethrin (α-CYP) is one of the most widely used insecticides. It may become an air pollutant and adversely affect the health. The present study was designed to determine whether treatment with N-acetyl cysteine (NAC), a well-known antioxidant, can be useful for the management of the deleterious effects of α-CYP on lung tissues. For this purpose, thirty two male rats were divided into four different groups (eight rats for each). Group (I) gavaged with corn oil (control group), group (II) gavaged daily with NAC (150 mg kg(-1) body weight), group (III) gavaged with α-CYP (14.5 mg kg(-1) body weight/day, dissolved in corn oil), group (IV) gavaged with NAC then with α-CYP 2 h later for 12 weeks. α-CYP significantly increased serum lactate dehydrogenase (LDH) and pulmonary malondialdehyde (MDA) levels, while decreased the activities of catalase (CAT) and superoxide dismutase (SOD) as well as reduced glutathione (GSH) content in lung. It also provoked higher levels of serum nitric oxide (NO), lung interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), hydroxyproline (Hyp) as well as heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-К B) gene expression in lung tissues. Histopathological alterations in lung with congestion, cellular infiltration, necrotic changes and thickening of inter-alveolar septa were observed following α-CYP administration. NAC reduced the adverse effects of α-CYP on lung tissues and improved the histological architecture of lung since it showed antioxidant, anti-inflammatory and antifibrotic effects on lung tissues. Our results indicate that NAC exerts a potent protective effect against α-CYP-induced oxidative damage and inflammation in lung tissues.

Inhibition of lung tumor development by berry extracts in mice exposed to cigarette smoke

Cigarette smoke (CS) and dietary factors play a major role in cancer epidemiology. At the same time, however, the diet is the richest source of anticancer agents. Berries possess a broad array of health protective properties and were found to attenuate the yield of tumors induced by individual carcinogens in the rodent digestive tract and mammary gland but failed to prevent lung tumors induced by typical CS components in mice. We exposed whole-body Swiss ICR mice to mainstream CS, starting at birth and continuing daily for 4 months. Aqueous extracts of black chokeberry and strawberry were given as the only source of drinking water, starting after weaning and continuing for 7 months, thus mimicking an intervention in current smokers. In the absence of berries, CS caused a loss of body weight, induced early cytogenetical damage in circulating erythrocytes and histopathological alterations in lung (emphysema, blood vessel proliferation, alveolar epithelial hyperplasia and adenomas), liver (parenchymal degeneration) and urinary bladder (epithelial hyperplasia). Both berry extracts inhibited the CS-related body weight loss, cytogenetical damage, liver degeneration, pulmonary emphysema and lung adenomas. Protective effects were more pronounced in female mice, which may be ascribed to modulation by berry components of the metabolism of estrogens implicated in lung carcinogenesis. Interestingly, both the carcinogen and the chemopreventive agents tested are complex mixtures that contain a multitude of components working through composite mechanisms.

A comparative ultrastructural and biochemical study between the effects of chlorphentermine and phentermine on rat lung

Morphological examination of lungs obtained from rats given a 60-mg/kg dose of the anorexigenic agent, chlorphentermine, revealed the presence of large macrophages resting mainly on the alveolar walls 24 hr after treatment. Continuation of daily chlorphentermine administration for 3 days increased the number of both free and alveolar-attached macrophages, and a progressive rise in the amount of these cells was noted until a peak was reached by 1 week, at which time the majority of these pulmonary cells floated freely in the alveolar lumen. Ultrastructural investigation showed that the cytoplasm of the macrophages contained a large amount of multilamellar bodies. Some of the type II alveolar epithelial cells contained a greater than normal quantity of multilamellar bodies, and these were also observed in some of the alveolar type I and bronchial epithelial cells. An interesting finding was the presence of remaining portions of junctional complexes on the surface of the free hypertrophied macrophages. In contrast, the pharmacologically similar agent, phentermine (60 mg/kg/day), produced no significant histopathological alterations in lung at 1, 3, 5, or 7 days after treatment. The observed chlorphenterminestimulated increase in pulmonary cells was associated with significant elevation in the incorporation of [ 14C]thymidine into DNA after 5 days, and an approximate three-fold increase in nucleic acid synthesis occurred after 1 week. Similarly, chlorphentermine administration augmented the incroporation of [ 14C]orotic acid into lung RNA both 1 and 3 days after treatment with a return to control values noted by 1 week. Enhancement in the biosynthesis of RNA was accompanied by a rise in the endogenous tissue levels of putrescine, spermidine, and spermine at various time periods examined; in general, maximal increases in the triad of polyamines were observed after 24 hr. In addition, anorectic drug administration elevated the concentration of pulmonary cyclic AMP after 3, 5, and 7 days with the highest quantitative change (183% of control values) seen after 72 hr. In contrast, treatment with phentermine produced either a marked decrease or lack of any significant alteration in the ability of lung to incroporate [ 14C]thymidine into DNA and [ 14C]orotic acid into RNA as well as in the levels of putrescine, spermidine, spermine, and cyclic AMP. Evidence indicates that, in the case of chlorphentermine, a positive relationship exists between pulmonary histiocytic proliferation and augmented nucleic acids synthesis, which may be associated with and is probably triggered by an initial stimulation of cyclic AMP and polyamine formation.