Protective effect of chitosan treatment against acetaminophen-induced hepatotoxicity

Acetaminophen (APAP) is the most commonly reported toxic ingestion in the world. Severe liver injury resulting from overdose or chronic use of APAP remains a significant clinical problem. In recent years, the mechanisms underlying liver injury caused by APAP have become much better understood. We have studied the protective effect of chitosan supplementation against APAP-induced hepatotoxicity with respect to changes in the levels of total and lipidbound sialic acid in the serum and in the liver tissue and changes in the activity of diagnostic marker enzymes, lipid peroxidation, and ceruloplasmin oxidase enzyme in normal and experimental groups of rats. During the experimental period, chitosan (200 mg/kg body weight per day) was administered to APAP þ chitosan-treated rats by oral gavage. Results showed that treatment with APAP induced a significant increase in the serum alanine aminotransferase and alkaline phosphatase activities, in total and lipid-bound sialic acids levels, and in the liver lipid peroxide content. The administration of chitosan significantly prevented APAP-induced alterations in the levels of diagnostic marker enzymes, total sialic acid, lipid-bound sialic acid, and malondialdehyde in the experimental groups of rats. Furthermore, chitosan administration increased the activity of ceruloplasmin oxidase. In conclusion, our results suggest that chitosan has a protective effect on APAP-induced hepatic injury in rats. The study sheds light on the therapeutic potential of chitosan in an APAP-induced hepatotoxicity model

The Effect of Antioxidant Astaxanthin on Intestinal Ischemia Reperfusion Damage in Rats

Background Mesenteric ischemia is a frequently encountered disease in surgical clinics, difficult to diagnose, and very mortal if not treated. Our study investigated the effects of astaxanthin, which is known to have potent antioxidant properties and is also known to have anti-inflammatory effects on ischemia-reperfusion (I/R) injury. Methods A total of 32 healthy Wistar albino female rats were used in our study. Subjects were randomized and equally divided into 4 groups; control (laparotomy group only), I/R (transient mesenteric ischemia group only), astaxanthin 1 mg/kg and 10 mg/kg doses. The transient ischemia time was 60 minutes and the reperfusion time was 120 minutes. Tissue samples were taken from intracardiac blood and terminal ileum after reperfusion. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) from blood samples, interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNFα), Caspase-3, P53 tests from terminal ileum were studied. Tissue samples were also taken for histopathological evaluation. Results At the end of the study, both doses of astaxanthin were found to significantly reduce MDA level, CAT, and SOD enzymatic activity, whereas higher doses of astaxanthin significantly reduced MDA level, CAT, and SOD enzyme activities. In addition, cytokines such as TNFα, IL-1 and IL-6 were found to be reduced at both doses of astaxanthin, but only significantly inhibited at higher doses. We observed that inhibition of apoptosis reduced caspase-3 activity and P53 and deoxyribonucleic acid (DNA) fragmentation. Conclusion Astaxanthin, a potent antioxidant, and anti-inflammatory, significantly reduces ischemia and reperfusion injury, especially when used at a dose of 10 mg/kg. These data need to be confirmed by larger animal series and clinical studies

Genotyping of acineto bacter baumanni isolates from patients with severe sepsis in anesthesia intensive care unit

15th World-Federation-of-Societies-of-Anaesthesiologists (WFSA) World Congress of Anaesthesiologists -- MAR 25-30, 2012 -- Buenos Aires, ARGENTINAWOS: 000302299100161…World Federat Soc Anaesthesiol (WFSA

Erythropoietin Protects the Kidney by Regulating the Effect of TNF-α in L-NAME-Induced Hypertensive Rats

Background/Aims: Hypertension is the leading cause of death worldwide. Chronic high blood pressure induces inflammation. Tumor necrosis factor (TNF)-α plays a major role in inflammation and also depresses the synthesis of erythropoietin, which exerts protective effects on tissue; however, the mechanism is still unclear. We investigated the protective effect of erythropoietin against tissue damage caused by hypertension in the kidney and whether this effect was suppressed by TNF-α. Methods: First, we detected the optimum chronic dose for darbepoetin-α (Depo), which is a long-acting erythropoietin analog for rats. We separated 60 female adult rats into 6 groups: control, Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), L-NAME+Depo, L-NAME+Remicade (an anti-TNF-α antibody), L-NAME+Depo+Remicade, Depo, and control. After 1 month of treatment, we measured cardiovascular parameters, took blood samples, sacrificed the rats, and removed kidneys for analyses. Results: The apoptotic index and the plasma and kidney mRNA levels of TNF-α increased in the L-NAME group and decreased in all other treatment groups. Macrophage accumulation increased in the L-NAME and L-NAME+Remicade groups, while it decreased in the Depo group. The mRNA abundance of TNF receptor 1 (TNFR1) decreased slightly in the Depo group and TNFR2 increased significantly in the same group. Conclusion: Erythropoietin protects kidney tissue against hypertension by preventing the apoptotic effects of TNF-α by blocking macrophage accumulation, decreasing TNF-α levels, and switching the TNF-α receptors from the apoptotic receptor TNFR1 to the proliferative receptor TNFR2

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by real-time polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and anti-apoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent