Hepatoprotective effects of Nigella sativa L and Urtica dioica L on lipid peroxidation, antioxidant enzyme systems and liver enzymes in carbon tetrachloride-treated rats

AIM： To investigate the effects of Nigella sativa 1 （NS） and Urtica dioica 1 （UD） on lipid peroxidation, antioxidant enzyme systems and liver enzymes in CCl4-treated rats. METHODS： Fifty-six healthy male Wistar albino rats were used in this study. The rats were randomly allotted into one of the four experimental groups： A （CCl4-only treated）, B （CCl4＋UD treated）, C （CCl4＋NS treated） and D （CCl4＋UD＋NS treated）, each containing 14 animals. All groups received CCl4 （0.8 mL/kg of body weight, sc, twice a week for 60 d）. In addition, B, C and D groups also received daily i.p. injections of 0.2 mL/kg NS or/and 2 mL/kg UD oils for 60 d. Group A, on the other hand, received only 2 mL/kg normal saline solution for 60 d. Blood samples for the biochemical analysis were taken by cardiac puncture from randomly chosen-seven rats in each treatment group at beginning and on the 60th d of the experiment. RESULTS： The CCl4 treatment for 60 d increased the lipid peroxidation and liver enzymes, and also decreased the antioxidant enzyme levels. NS or UD treatment （alone or combination） for 60 d decreased the elevated lipid peroxidation and liver enzyme levels and also increased the reduced antioxidant enzyme levels. The weight of rats decreased in group A, and increased in groups B, C and D. CONCLUSION： NS and UD decrease the lipid peroxidation and liver enzymes, and increase the antioxidant defense system activity in the CCl4-treated rats.

Comparative Assessment of Melatonin-Afforded Protection in Liver, Kidney and Heart of Male Mice against Doxorubicin Induced Toxicity

Melatonin (MEL) was investigated for protection against the anthracycline antibiotic doxorubicin (Dox) that is well known for its oxidative damage to various body organs. It was aimed to have a comparison of this protection to heart, liver and kidney in the treated subjects. In this study, groups of mice were treated with Dox and melatonin and their individual or combined effects were evaluated by assessing lipidperoxidation, non-protein sulfhydryls (NP-SH) and nitrate/nitrite (NO) contents in these tissues. Plasma aminotransferases, LDH and CK-MB enzyme activities were measured. Moreover, these tissues were subject to histopathological assessment. MEL co-treatment significantly prevented any rise in lipidperoxides more significantly in heart and liver as compared to kidney. In tandem, MEL prevented a decline in GSH that was observed by Dox alone in liver and kidney. Dox significantly increased total NO levels in all the tissues. Melatonin at both dose levels could not afford protection against nitrosative stress. MEL in combination treatment provided significant

Lipid peroxidation injury after percutaneous coronary intervention and its clinical effects in patients with coronary artery disease complicated with hypertension

Background Percutaneous coronary intervention （PCI） is a way of treating patients with coronary artery disease （CAD）, especially for those with acute coronary syndrome （ACS）. Previous studies have proved that the main complication of PCI is the injury caused by lipid peroxidation. The pathophysiology of lipid peroxidation is that with the revascularization of blocked coronary arteries by PCI, external oxygen enters the ischemic myocardial cells. As the activity of oxygen free radical scavenging enzyme decreases, oxygen free radicals are produced, resulting in lipid peroxidation damage on myocardial cell membrane. This study investigated the influence of hypertension （HBP） on PCI-induced lipid peroxidation in CAD patients. Methods Seventy patients with CAD were divided two groups： group A including 32 patients with CAD, and group B including 38 patients with CAD complicated with HBP. All patients received PCI. The plasma levels of malonaldehyde （MDA） and superoxide dismutase （SOD） were measured before PCI and 20 minutes, 24 hours, and 7 days after PCI respectively. The patients were followed up for cardiac events after PCI for 6 momths. Results The plasma levels of SOD and MDA were increased in both groups after PCI, but these changes were more in group B. On the 7th day the levels of SOD and MDA remained high in group B, whereas retained to the pre- operational levels in group A. During the follow-up of 6 months after the PCI, 4 patients were found to suffer from coronary restenosis, including one patient in group A （3.1%）, and 3 patients in group B （7.8%）. Conclusions The results suggest that PCI induces short-time free radical production in patients with CHD, especially in those complicated with HBP.