| Background: It is realized recently that liver fibrosis plays an important role in the generation and development of chronic hepatic disease and cirrhosis. It is conformed that the mechanism of liver fibrosis is the synthesis increased in extracellular matrix (ECM) proteins of liver cells and their degradation decreased or both. This process is mainly due to active the HSC by interaction between liver cells, and liver cells with ECM mediated by cytokines. The cytokine may play a part in the pathogenesis fibrosis in chronic hepatic damage that can active HSC. Recently amounts data from experiment and clinic have proved that LPO can active HSC and enhance the synthesis of ECM and result in hepatocyte injury. So it has become very important to prevent liver fibrosis with anti-oxidation agent. Garlicin as an anti-oxidation agent has the effective hepato-protection funtion on ethanol-induced hepatoeoxicity, which is related to its selective effect on the glutathione-related enzyme system. It has been used to resistant the carcinoma and atherosclerosis.Objective: In this paper the effect on liver fibrosis of Garlicin and its mechanism in experimental rats was studied by which the marked SGPT, SCOT, CHOL, TG, HA, LN, PHINP, P I NP, TGF- P j, TNF- a , IL-6, IL-10 were observed.Method: Liver fibrosis model in rats was established by using DMN. 56 Sprague-Dawley rats were randomly divided into seven groups: normal group, Garlicin low and middle dose (llmg/kg.d, 22mg/kg.d) of preventive groups and middle dose (22mg/kg.d) of treatment group, as well as Colchincine (0.15mg/kg.d) and Bupleurum mixture (6g/kg.d) positive control groups. Except for normal group, other six groups were injected interperitoneally dimethynitrosamine (DMN) at dose of 10mg/kg.ea. It was totally injected for 10 times. Rats in the middle dose of treatment group were treated with Garlicin three weeks after model started. Other groups were treated with drugs at the same time when model group started Thetreatment was consecutively carried out for 42 days. After the last time of treatment, rats were anaesthetized by 3% Pentobarbital Sodium, the celiac arterial blood of all rats was taken. The serum levels of hyaluronic acid, laminin, and procollagentype I and III, as well as liver function and cytokines were analyzed. Histological examination was also performed. Results:1. In groups treated with Garlicin, serum levels of SGPT and SCOT were reduced Albumin was increased significantly (P<0.01 or P<0.05). The treatment group with middle dose of Garlicin has the most significant effect on SGPT and SCOT. But the groups treated with Colchincine and Bupleurum mixture did not exert any effect on liver function improved (p>0.05). Besides, TG and CHOL were decreased in the low and middle dose groups. The histological examination showed that the lesion, congestion, hemorrhagic and accumulation of TG in the liver of Garlicin preventive groups were less severe than that in the model group and positive control group. Electronic microscope results showed that in preventive group treated with Garlicin the liver necrosis and lesion were less severe than that in the model group. The liver cells in the middle dose of preventive group were as normal as negative control group. It is suggested that Garlicin can prevent the hapatocytes from injury.2. In the low and middle dose of Garlicin preventive and treatment groups serum levels of HA, LN, PINP, PHINP were remarkably reduced (p<0.05 or P<0.01) especially in PIUNP. Depositions of reticular fibrin and collagen fibrin were studied in liver section by immunehistochemical technique with special antibody. The area of fibrin was analyzed with SSS. The data showed that Garlicin was able to decrease the accumulation of collagen and reticular fibrin, especially in collagen fibrosis. Prominent differences between Garlicin groups and model group were existed (p<0.01, PO.05). Electronic microscope results showed that depositions of collagen between liver cells and Disse cells were less severe than that in the model grou...
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