Ahmet Guzel

Protective effect of curcumin on acute lung injury induced by intestinal ischaemia/reperfusion

The aim of this study is to evaluate the role of curcumin on acute lung injury induced by intestinal ischaemia/reperfusion (I/R). A total of 30 male Wistar albino rats were divided into 3 groups: sham, I/R, and I/R + curcumin; each group contains 10 animals. Sham group animals underwent laparotomy without I/R injury. After I/R groups animals underwent laparotomy, 1 h of superior mesenteric artery ligation were followed by 1 h of reperfusion. In the curcumin group, 3 days before I/R, curcumin (100 mg/kg) was administered by gastric gavage. All animals were killed at the end of reperfusion and lung tissue samples were obtained for biochemical and histopathological investigation in all groups. To date, no more biochemical and histopathological changes on intestinal I/R injury in rats by curcumin treatment have been reported. Curcumin treatment significantly decreased the elevated tissue malondialdehyde levels and increased reduced superoxide dismutase, and glutathione peroxidase enzyme activities in lung tissue samples. Intestinal I/R caused severe histopathological injury including oedema, haemorrhage, increased thickness of the alveolar wall, and infiltration of inflammatory cells into alveolar spaces. Curcumin treatment significantly attenuated the severity of intestinal I/R injury. Furthermore, there is a significant reduction in the activity of inducible nitric oxide synthase and increase in the expression of surfactant protein D in lung tissue of acute lung injury induced by intestinal I/R with curcumin therapy. It was concluded that curcumin treatment may have beneficial effects in acute lung injury, and therefore has potential for clinical use.

Anti-inflammatory and antioxidant effects of infliximab in a rat model of intestinal ischemia/reperfusion injury.

The aim of this study was to investigate the possible protective effects of infliximab on oxidative stress, cell proliferation and apoptosis in the rat intestinal mucosa after ischemia/reperfusion (I/R). A total of 30 male Wistar albino rats were divided into three groups: sham, I/R and I/R+ infliximab; each group comprised 10 animals. Sham group animals underwent laparotomy without I/R injury. I/R groups after undergoing laparotomy, 1 hour of superior mesenteric artery ligation occurred, which was followed by 1 hour of reperfusion. In the infliximab group, 3 days before I/R, infliximab (3 mg/kg) was administered intravenously. All animals were killed at the end of reperfusion and intestinal tissues samples were obtained for biochemical and histopathological investigation in all groups. To date, no biochemical and histopathological changes have been reported regarding intestinal I/R injury in rats due to infliximab treatment. Infliximab treatment significantly decreased the elevated tissue malondialdehyde levels and increased reduced superoxide dismutase and glutathione peroxidase enzyme activities in intestinal tissues samples. I/R caused severe histopathological injury including mucosal erosions, inflammatory cell infiltration, necrosis, hemorrhage, and villous congestion. Infliximab treatment significantly attenuated the severity of intestinal I/R injury, inhibiting I/R-induced apoptosis, and cell proliferation. Because of its anti-inflammatory and antioxidant effects, infliximab pretreatment may have protective effects on the experimental intestinal I/R model of rats.

Infliximab attenuates activated charcoal and polyethylene glycol aspiration-induced lung injury in rats

ABSTRACT Aspiration is a serious complication of gastrointestinal (GI) decontamination procedure. Studies have shown that tumor necrosis factor-α (TNF-α) blockers have beneficial effects on lung injury. Therefore, the authors investigated the attenuation by infliximab (INF) on activated charcoal (AC)- and polyethylene glycol (PEG)-induced lung injury in rat model. Forty-two male Sprague-Dawley rats were allotted into 1 of 6 groups: saline (NS), activated charcoal (AC), polyethylene glycol (PEG), NS+INF treated, AC+INF treated, and PEG+INF treated. All materials were aspirated into the lungs at a volume of 1 mL/kg. Before aspiration, the rats were injected subcutaneously with INF. Seven days later, both lungs and serum specimens in all groups were evaluated histopathologically, immunohistochemically, and biochemically. Following aspiration of AC and PEG, evident histopathological changes were assigned in the lung tissue that were associated with increased expression of inducible nitric oxide synthase (iNOS), increased serum levels of oxidative stress markers (malondialdehyde [MDA], surfactant protein-D [SP-D], TNF-α), and decreased antioxidant enzyme (glutathione peroxidase [GSH-Px]) activities. INF treatment significantly decreased the elevated serum MDA and TNF-α levels and increased serum GSH-Px levels. Furthermore, the current results show that there is a significant reduction in the activity of iNOS in lung tissue and increased serum SP-D levels of AC and PEG aspiration-induced lung injury with INF treatment. These findings suggest that INF attenuates lung inflammation and prevents GI decontamination agent–induced lung injury in rats.

The effects of α-tocopherol on oxidative damage and serum levels of Clara cell protein 16 in aspiration pneumonitis induced by bile acids.

Our aim in this study is to examine the effects of α-tocopherol (AT) on rats with aspiration pneumonitis induced with bile acids (BAs). The animals were divided in to four groups, namely saline group (n = 7), saline + AT group (n = 7), BA group (n = 7), and BA + AT group (n = 7). Saline and BA groups aspirated intratracheally with 1 ml/kg saline and 1 ml/kg bile acids, respectively. AT was given at 20 mg/kg/day dosage for 7 days to the groups. AT group was given 20 mg/kg/day AT for 7 days. Malondialdehyde (MDA), Clara cell protein 16 (CC-16), catalase (CAT), superoxide dismutase (SOD), as well as peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar edema, alveolar exudate, alveolar histiocytes, and necrosis were evaluated. The CAT activity of the BA group was significantly lower than the saline group. In the BA + AT group, there was a significant increase in SOD and CAT activities when compared with that of the BA group. The CC-16 and MDA contents in the BA group were significantly higher than in the saline group. The CC-16 and MDA levels of the BA + AT group were significantly lower than BA group. Histopathologic changes were seen in BA group, and there was a significant decrease in the BA + AT group. In conclusion, AT might be beneficial in the treatment of aspiration pneumonitis induced by BAs because AT decreased oxidative damage and resulted in a decrease in CC-16 levels.

Severe Carbamazepine Intoxication in Children: Analysis of a 40-Case Series

Background We compared the factors that might impact the severity and the prognosis of carbamazepine (CBZ) intoxication in children, as well as the efficacy levels of the treatment options. Material/Methods Demographic information and clinical and laboratory findings for 40 patients were evaluated retrospectively. Predictive parameters for the development of serious complications were studied. Results Median age of patients was 14 years; 65% of the patients were female. The most common pathological clinical finding and laboratory abnormality were inability to awaken the patient and hyperglycemia (45% and 60%, respectively). The incidences of convulsion, coma, and respiratory failure were 14 (35%), 10 (25%), and 3 (7.5%), respectively. The Glasgow Coma Scale (GCS) scores and pH levels at emergency service admission were significantly lower in the severe intoxication group and the ICU admission group, and body temperature and serum glucose and lactate levels were significantly higher in these groups. A significantly negative correlation was found between the serum CBZ level and the GCS score, but the serum CBZ level was found to be significantly positively correlated with the lactate level. Conclusions According to our study, the GCS score at admission to hospital, the serum CBZ, glucose, pH, and lactate levels, and body temperature might be useful in predicting serious CBZ intoxication and prognosis in pediatric cases. We conclude that invasive treatment methods, such as hemodialysis or albumin-enhanced continuous venovenous hemodialysis, should be used in patients who do not respond to supportive treatment.

Can empirical hypertonic saline or sodium bicarbonate treatment prevent the development of cardiotoxicity during serious amitriptyline poisoning? Experimental research.

Summary Objective The aim of this experimental study was to investigate whether hypertonic saline or sodium bicarbonate administration prevented the development of cardiotoxicity in rats that received toxic doses of amitriptyline. Method Thirty-six Sprague Dawley rats were used in the study. The animals were divided into six groups. Group 1 received toxic doses of i.p. amitriptyline. Groups 2 and 3 toxic doses of i.p. amitriptyline, plus i.v. sodium bicarbonate and i.v. hypertonic saline, respectively. Group 4 received only i.v. sodium bicarbonate, group 5 received only i.v. hypertonic saline, and group 6 was the control. Electrocardiography was recorded in all rats for a maximum of 60 minutes. Blood samples were obtained to measure the serum levels of sodium and ionised calcium. Results The survival time was shorter in group 1. In this group, the animals’ heart rates also decreased over time, and their QRS and QTc intervals were significantly prolonged. Groups 2 and 3 showed less severe changes in their ECGs and the rats survived for a longer period. The effects of sodium bicarbonate or hypertonic saline treatments on reducing the development of cardiotoxicity were similar. The serum sodium levels decreased in all the amitriptyline-applied groups. Reduction of serum sodium level was most pronounced in group 1. Conclusion Empirical treatment with sodium bicarbonate or hypertonic saline can reduce the development of cardiotoxicity during amitriptyline intoxication. As hypertonic saline has no adverse effects on drug elimination, it should be considered as an alternative to sodium bicarbonate therapy.

Analysis of the Protective Biochemical and Pathologic Effects of Aminoguanidine on an Experimental Aspiration Pneumonitis Model Induced by Bile Acids

BACKGROUND Gastroesophageal reflux (GER) is a common clinical pathology detected in childhood. Bile acids (BAs) are present in reflux and cause various pathologies in the esophagus, the larynx, and the lungs. OBJECTIVE We aimed to show if aminoguanidine (AG) contributes to the biochemical and histopathologic treatment of experimental aspiration pneumonitis induced by BAs. METHODS Twenty-eight female Sprague Dawley rats were used. There were 4 groups in the study: (1) group aspirated with 0.9% saline (n = 7), (2) group aspirated with 0.9% saline and treated with AG (n = 7), (3) group aspirated with a solution of 10 mg/kg taurocholic acid and 5 mg/kg taurochenodeoxycholate (n = 7), and (4) group aspirated with BA and treated with AG (n = 7). The saline and BA solutions were administered as 1 mL/kg intratracheally. The AG was administered intraperitoneally twice a day at a 150 mg/kg dose for 7 days. The different histopathologic and biochemical parameters were analyzed. RESULTS Clara cell protein 16 and malondialdehyde levels were found to be significantly higher in the BA group than in the group where saline was administered; however, they were significantly lower in the BA + AG group than in the BA group. The total superoxide dismutase activity decreased significantly in the BA group compared with the group where saline was administered. A significant increase in superoxide dismutase activity was observed in the BA + AG group when compared with the group where only BA was administered. When the group where BA was administered solely was compared with the group where saline was administered, peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar histiocytes, interstitial fibrosis, and granuloma were significantly higher in the BA group than in the saline group. When the BA + AG group was compared with the BA group, peribronchial inflammatory cell infiltration, alveolar septal infiltration, alveolar histiocytes, interstitial fibrosis, and granuloma were found to be significantly lower. CONCLUSIONS Oxidant stress increases and antioxidant capacity decreases in pneumonitis induced by BAs. AG administration as an antioxidant helps in recovery, both biochemically and histopathologically. Consequently, AG seems to be an alternative that should be considered in a conservative approach to treating aspiration pneumonitis.