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1.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-258472

ABSTRACT

Both Patrinia Herba and Patrinia Radix are traditional Chinese herbal medicines. The herbal source and medicinal part of them are confusing in the herbal medicine market of China. To explore the evolution and transition of the herbal source and medicinal part of Patrinia Herba and Patrinia Radix, this paper systematically summarizes the record of the herbal source and medicinal part of them in ancient classics of herbal medicine in China. According to the findings, before Ming Dynasty, Patrinia Herba originated from the radix of the plants with yellow flowers of Patrinia. In Ming and Qing Dynasty, Patrinia Herba originates from the whole plant (including the radix)of the plant with white flowers of Patrinia. In Ming Dynasty, Patrinia Radix, stemming from the radix of the plants with yellow flowers of Patrinia, started to be used as a traditional Chinese herbal medicine, which had the same herbal source with that of Patrinia Herba before Ming Dynasty. Therefore, Patrinia Herba and Patrinia Radix can be seen as the same traditional Chinese herbal medicine, and the genuine of Patrinia Herba should be the radix and the whole herba of P. scabiosaefolia and P. heterophylla.

2.
World J Gastroenterol ; 11(32): 4957-61, 2005 Aug 28.
Article in English | MEDLINE | ID: mdl-16124045

ABSTRACT

AIM: To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells (HSCs), in acute liver injury induced by CCl(4), and to explore their role in the recovery from hepatic fibrosis phase. METHODS: An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride (0.3 mL/100 g body weight) twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. The rats from the intervention group were fed with chow supplemented with vitamin E (250 mg/kg) and selenium (0.2 mg/kg), and the rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by alpha-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL) and alpha-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS: In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION: Vitamin E and selenium supplementation at the given level can inhibit CCl(4)-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , Chemical and Drug Induced Liver Injury/drug therapy , Selenium/pharmacology , Vitamin E/pharmacology , Animals , Carbon Tetrachloride , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Dietary Supplements , Drug Therapy, Combination , Male , Rats , Rats, Sprague-Dawley
3.
Wei Sheng Yan Jiu ; 34(2): 194-6, 2005 Mar.
Article in Chinese | MEDLINE | ID: mdl-15952662

ABSTRACT

OBJECTIVE: Effects of dietary supplementation of vitamin E and selenium on proliferation and apoptosis of activated hepatic stellate cell(HSC) were investigated in the rat model of liver fibrosis induced by intraperitoneal injection with CCl4. METHODS: Activated HSC was determined by alpha-smooth muscle actin immunohistochemistry staining and apoptotic HSC determined by dual staining both of the terminal deoxynucleotidyl transferase UTP nick end labeling(TUNEL) and of alpha-smooth muscle actin immunohistochemistry. RESULT: During fibrosis recovery, the number of activated HSCs both in pathological group and in intervention group went down gradually,meanwhile, both the number of apoptotic HSCs and the collagen liver also descend little by little. These data confirmed that HSCs had the core effect on liver fibrogenesis and apoptosis may be a major factor regulating HSCs numbers during the injury-fibrosis-recovery sequence. At each time point, the number of activated HSCs in pathological group is more than intervention group, while apoptotic HSCs are less, which suggested dietary supplement with antioxidative nutrients had effect on HSC apoptosis but more studies are necessary to make the mechanism clearer. CONCLUSION: Dietary supplement with proper vitamin E and selenium can effectively lighten the hepatic fibrosis and promote the recovery of hepatocyte and the degradation of the existing collagens, ie, it is beneficial to the recovery of hepatic fibrosis.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , Hepatocytes/drug effects , Liver Cirrhosis, Experimental/pathology , Animals , Carbon Tetrachloride , Cell Proliferation/drug effects , Dietary Supplements , Liver Cirrhosis, Experimental/drug therapy , Male , Rats , Rats, Sprague-Dawley , Selenium/pharmacology , Vitamin E/pharmacology
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