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Cirrhosis of the liver lipid peroxidation in plasma and erythrocyte superoxide dismutase Clinical significance


O level,[link widoczny dla zalogowanych], the former is 6.93.48, closely related. The latter was 7.89 ± 4.2, but no difference between the two groups of patients with cirrhosis of the liver causes an increase in free radicals and endotoxin (p> O.05). Hyperlipidemia related. Due to liver dysfunction, intestinal levels of endotoxin in the red blood cell 8OD in liver cirrhosis patients were bases eB End phagocytic Kupffer cells Erzhi endotoxin 4245.22 ± 1448. ou / gHb, its value is lower than the normal hormone blood. Studies have shown that endotoxin free radicals not only cheaper Hepatology Pro i0 1994 No. 2 production increased in the liver cells, but also to Ca the increase in free radicals caused by toxins mechanism. intracellular calcium overload by activation of phospholipase, cyclooxygenase, and then by the lipoxygenase pathway generates prostaglandins, leukotrienes and free radicals and other active substances to cells further damage. Free base damage caused by membranous organelles increase in membrane Ca permeability, intracellular calcium overload re-activation of phospholipase and lipid peroxidation, the ongoing vicious circle, leading to cell damage or even death. In addition, patients with cirrhosis of the liver antioxidant function, and free radical scavenging by the disorder, the patient blood S0D,[link widoczny dla zalogowanych], selenium levels in the skin glutathione peroxidase (GSH - PX) activity F down on. Selenium is an essential component of GSH-PX. Because antioxidant enzymes and antioxidants can capture and remove free radical, it has a protective effect on liver cells. Commonly used in clinical drugs such as vitamin E, glutathione, selenium, coenzyme Q, alcohol and medicine allopurinol Chuanxiong Ridge, Salvia, Angelica a 83 and so on. Group I patients with liver cirrhosis, 16 with vitamin E down 1 to 2 months after treatment,[link widoczny dla zalogowanych], 62.5 (1O/16 cases) compared with plasma LPO levels before treatment decreased 2.10ttmol / L, while the difference between before and after treatment levels of non-S0D too. Can be assumed that treatment with anti-oxidants to reduce the LPO levels in the blood of patients to reduce free radical damage of liver cells, these drugs in the treatment of liver diseases in the position and role deserves further study. ● BIBLIOGRAP 1. ParksDAletai. Hepato [ogy1988; 8:6802. Christi Ⅱ ec, eta1. JLabclinmed1975: 85:33.7.3, Wan red Journal of Clinical Hepatobiliary pain. 1991; 7:200. . SakaguchIS. etal, MicrobiolImmanolL98; 28:517.5. SakaguchiS. eta1. MicrobiolImmuol1989; 83: g9.6MeyerFB, eta:. Mayoc1inproc1987: 62:35 uranium sheath, Qian beak brother , calcium Juan resistance, sunset Ao code free radical scavengers and calcium antagonists on liver damage and liver fibrosis in the protective effect Yin dead, the First Affiliated Hospital of Nanjing Medical University Fort Fort _ a Lv Xiuzhen Sun Hong ridge camera focuses on training the system to COl rat liver fibrosis | vote for radical scavenger SOD, CAT and calcium antagonists Ver, Nif, on both the liver cell damage and liver fibrosis role in the prevention and protection are compared. The results showed that CAT has more star tSOD song and lipid peroxidation, and thus the protective effect of liver cells to prevent the smell of the original quality of the fiber cavity proliferation, inhibition of hepatic fibrosis. While only a mild Ver lipid peroxidation, Nif ~ ll unperturbed lipid peroxidation t does not have the protection of the liver cell function. Both had no hepatic fibrosis. In recent years, free radical scavengers and calcium antagonists on the protective effect of liver cells by increasing clinical attention, some researchers even think that calcium antagonists with anti-hepatic fibrosis. Recently, the authors were also observed in the history of free radical scavengers have some experience of the prevention of liver fibrosis in rats. This study was designed on the free radical scavenger superoxide dismutase (SOD), catalase (CAT) and verapamil (Ver), nifedipine (Nif) in liver cell injury and hepatic fibrosis the process of prevention and protection were compared. Materials and Methods Male Wistar 60 rats, weighing 180 ~ 220g, were randomly divided into 6 groups; normal control group, CC1. Touch-type group,[link widoczny dla zalogowanych], SOD group,[link widoczny dla zalogowanych], CAT group, Ver group and the Nil group. In addition to the normal group, the other 5 groups to 2OCC1. Tuck body wax by 0.5ml/kg intraperitoneally, 2 times per week, continuously for 45 days. Each injection of CC1. At the same time and day of each component