Hydroclathrus clathratus as anti-damaging agent against lung injury in male albino rats

Purpose: Multiple organ failure, including acute lung injury, is a common complication of intestinal ischemia and reperfusion (I/R) injury and contributes to its high mortality rate. Activated polymorphonuclear neutrophils and reactive oxygen species contribute to the lung injury caused by intestinal I/R. Mineralokortikoid receptor antagonist spironolactone has a protective effect against I/R injury in animal models of retina, kidney, heart, and brain. The aim of the present study is to investigate the effect of aldosteron receptor blocker spironolactone on lung injury induced by intestinal I/R. Methods: Wistar albino rats were divided into four groups: (1) sham control; (2) intestinal I/R (30 min of ischemia by superior mesenteric artery occlusion followed by 3 h of reperfusion); (3) spironolactone pretreatment (20 mg/kg) + I/R; and, (4) spironolactone pretreatment without I/R. Spironolactone was given orally 3 days prior to intestinal I/R. A marker for lipid peroxidation (malondialdehyde; MDA), an indicator or oxidation state (reduced glutathione; GSH), an index of polymorphonuclear neutrophil sequestration (myeloperoxidase; MPO), inducible nitric oxide synthase (iNOS) immunoreactivity, and the histopathology of the lung tissue were analyzed. Results: Spironolactone pretreatment markedly reduced intestinal I/R-induced lung injury as indicated by histology and MDA and MPO levels. Moreover, the pretreatment decreased the iNOS immunoreactivity. Conclusion: The present study strongly suggests that spironolactone pretreatment decreased neutrophil infiltration, iNOS induction, oxidative stress, and histopathological injury in an experimental model of intestinal I/R induced-lung injury of rats.

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Protective role of caffeine versus N-acetylcysteine in hyperoxic acute lung injury in neonatal rats

Journal of Morphological Sciences ◽

10.4322/jms.113617 ◽

2017 ◽

Vol 34 (02) ◽

pp. 058-067

Author(s):

A. Sadek ◽

R. Khattab ◽

A. Amer ◽

A. Youssef

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Immune Reaction ◽

Interleukin 1 ◽

Protective Role ◽

High Oxygen ◽

Control Group ◽

Albino Rats ◽

Neonatal Rats

Abstract Introduction: Prolonged breathing of high oxygen concentration leads to hyperoxic acute lung injury. Neonatal Respiratory diseases usually require increased supplement of high oxygen concentrations, so neonates are more susceptible to hyperoxic acute lung injury. The aim of this work was to investigate the protective role of caffeine versus N-acetylcysteine against hyperoxic acute lung injury in neonatal rats. Materials and Methods: 32 albino rats aged seven days were used in this experiment. The pups were divided into four groups; 1) Control or normoxic group; rats placed in normoxic chamber where fraction of inspired oxygen (FiO2) was 0.21, 2) Hyperoxic group; rats were placed in hyperoxic chamber (FiO2>0.8) using an oxygen flow of 1.5 Litre/min, 3) Hyperoxia-CAF group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 20 mg/kg caffeine just prior to exposure, and 4) Hyperoxia-NAC group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 150 mg/kg N-acetylcysteine just prior to exposure. 48 hours after exposure, lung specimens were processed for histological and immunohistochemical study using caspase-3, cluster of differentiation-68-antibody (CD68) and interleukin-1-beta (IL-1β). Results: Neonatal hyperoxia led to severe impairment in lung architecture, with a highly significant increase in alveolar macrophages. Also, caspase and IL-1β immune-reaction were increased significantly as compared to control group. Caffeine could improve the histolopathological picture of hyperoxic acute lung injury, and also could decrease alveolar macrophage count and IL-1β immune-reaction better than N-acetylcysteine. Conclusion: Caffeine is more effective than N-acetylcysteine in prophylaxis against hyperoxic acute lung injury in neonates.

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Evaluation of the possible apitherapeutic value of bee venom and bee propolis on L-arginine-induced acute pancreatitis and lung injury in albino rats

International Journal of Molecular Biology ◽

10.15406/ijmboa.2020.05.00124 ◽

2020 ◽

Vol 5 (1) ◽

pp. 1-12

Author(s):

Noha Abd El Latif Ibrahim ◽

Sahar Bastawy Ahmed ◽

Aliaa Ali Hassan ◽

Nehad Ahmed Sadek ◽

Maha Khaled Abdelwahed

Keyword(s):

Acute Pancreatitis ◽

Lung Injury ◽

Bee Venom ◽

Albino Rats

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Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

Clinical & Investigative Medicine ◽

10.25011/cim.v31i5.4870 ◽

2008 ◽

Vol 31 (5) ◽

pp. 242 ◽

Cited By ~ 22

Author(s):

Oguz Galip Yildiz ◽

Serdar Soyuer ◽

Recep Saraymen ◽

Celalettin Eroglu

Keyword(s):

Radiation Therapy ◽

Lung Injury ◽

Caffeic Acid ◽

Radiation Treatment ◽

Caffeic Acid Phenethyl Ester ◽

Albino Rats ◽

Protective Effects ◽

Sod Activity ◽

Radiation Induced

Purpose: The prevention of radiation-induced pulmonary toxicity may help to improve radiation therapy in the cancer patient. The aim of this study was to investigate the pulmonary protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on radiation-induced lung injury in rats. Methods:30 Wistar albino rats were divided into three groups and treated with saline, Radiation (RT) and RT + CAPE respectively. All rats were treated with CAPE (50 ?mol/kg i.p.) or saline. The first dose of CAPE was injected 24 h before radiation and application continued daily, with radiation in second day and 2 days more after the radiation treatment. Radiation dose was 800 cGy for total body. At 72 hr after the last radiation application, under general anesthesia using ip ketamine, the lungs were removed immediately after decapitation. After sacrification, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) activities and malondiadehyde (MDA) levels were evaluated in lung tissue. Results: The level of malondialdehyde (MDA) was higher in the RT group (233.4±1.5 nmol/g protein) than in both the control (131.8±0.92) and the RT + CAPE (151.4±1.8) groups (P < 0.001). However, CAT activity was decreased in the RT group (7.26±0.27 Umg protein) compared with control (8.49±0.51) and increased again in the RT + CAPE group (8.31±0.56; P < 0.001). In accord with CAT activity, SOD activity in the RT group (0.42±0.07 nmolMDA/g wet tissue) was different from the control (0.78±0.02) and RT + CAPE (0.86±0.06) groups (P < 0.001). Conclusion: CAPE aplication with radiation therapy attenuated radiation induced pulmonary injury in vivo, possibly by its antioxidant effect.

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