| Hepatic fibrosis is a process of repair response to the liver injury, and involves the abnormal accumulation of collagen, degeneration and necrosis of hepatocytes, and damage to liver architecture and function. It has been proved by clinical research and experimental work on animals that hepatic fibrosis is the key process in the conversion of chronic liver disease into liver cirrhosis. Hepatic fibrosis is a reversible process, and can be resorted to health through various ways such as suppressing the inflammation reaction, inhibiting the excessive synthesis of collagen, and accelerating the degradation of collagen by enhancing the activities of collagenase. Today much attention has been paid to anti-fibrosis procedure in the treatment of chronic liver disease or prevention of liver cirrhosis, but seldom can a satisfying result be achieved in clinical practice due to the extremely complicated formation of hepatic fibrosis. Therefore finding eutherapeutic medicines has become an important task for pharmaceutical researchers to fulfil. We study the inhibitory effects of Phellinus igniarius (PI), a polyporus fungal medicine, on the experimental hepatic fibrosis, and further reveal the polyergic mechanism of its action. Hepatic injury was induced by CCl4 in rats. Histomorphology study showed that PI could prevent the degeneration of hepatocytes and proliferation of collagen in the liver. Serum levels of HA, LN and â…£-C from prophylactic group were reduced close to normal group (P>0.05), while the PCâ…¢ level was reduced to the value half of the model group (P<0.01). Levels of TBIL, ALT and AST were also declined significantly (P<0.05, P<0.01). The results showed that PI had an protective effect on the liver. It could also retard the progress of hepatic fibrosis and prevent the occurring and developing of chronic liver injury. The curative effect of PI on hepatic fibrosis was studied after administration of PI in high, median and low dosage to rats. High dosage (1.0g/100g body weight) of PI was very effective to cure hepatic fibrosis. It could significantly reduce the serum levels of collagen and various enzymes and relieve thesymptom of collagen accumulation in liver. Median dosage (0.5g/100g body weight) could also cure hepatic fibrosis though it was not as effective as high dosage. Low dosage (0.25g/100g body weight) had little effect on hepatic fibrosis and could only slightly reduce the serum levels of collagen and enzymes. The curative effect of PI suggested that PI had the potentiality to reverse hepatic fibrosis, and there existed a positive correlation between the efficacy and PI dosage. The mechanisms of PI inhibiting hepatic fibrosis were revealed on multiaspect because Chinese traditional medicine had many ingredients and involved in various pharmacological activities. 1. Hemorheological studies in rats displayed an intimated connection between hepatic fibrosis and hemorheological changes. When hepatic fibrosis was induced by CCl4, blood viscosity became high and erythrorheological ability became low, thus led to microcirculatory disturbance, which would aggravate hepatic injury. Compared with model group, the whole blood viscosity, reduced blood viscosity, hematocrit and red blood cell (RBC) rigidity in PI group were decreased obviously (P<0.01, P<0.05). The levels of ATPase and ChE in liver tissue were increased in PI group. Therefore it could be conclude that PI could protect the liver through meliorating hemorheological properties, improving blood circulation in liver and supplying sufficient nutrition for hepatocytes. 2. Lipid peroxidation plays an important role in the process of CCl4 inducing liver injury. As compared with model group, serum level of active oxygen in PI group significantly decreased (P<0.01), tissue level of SOD activity was elevated (P<0.10) and MDA content was decreased (P<0.20). However, the experiment in vitro on anti-photooxidation didn't provide any positive evidence of PI inhibiting oxygen free radicals. We infered that PI might prevent lipid...
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