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1.
Acta Pharmacol Sin ; 22(12): 1159-67, 2001 Dec.
Article in English | MEDLINE | ID: mdl-11749818

ABSTRACT

AIM: To study the prophylactic effects of four Chinese traditional prescriptions against experimental liver injury. METHODS: Liver toxins, alpha-naphthylisothiocyanate (ANIT), and carbon tetrachloride (CCl4) were used to induce acute liver injury. Simo Yin(SMY), Guizhi Fuling Wan (GFW), Xieqing Wan (XQW), and Sini San (SNS) were fed (500 mg/kg, in saline, po) to the rats before toxin administration. All the animals were killed 48 h after toxin insulted. Serum index of liver function and hepatic lipid peroxidation (LPO) were estimated. Histopathological observation was conducted simultaneously. RESULTS: The rats treated with ANIT exhibited elevations of serum total bilirubin (TBI), alkaline phosphatase (ALP), glutamate-oxalate- transaminase (GOT), glutamate-pyruvate-transaminase (GPT), as well as cholestasis and parenchyma necrosis. In rats, challenged with ANIT, receiving the pre-treatment of prescriptions of SMY, XQW, and SNS, the biochemical and morphological parameters of liver injury were significantly reduced. The increased LPO level in liver tissue, associated with the provoked serum GOT and GPT levels were the salient features observed in CCl4-insulting rats. Pre-treatment of four prescriptions showed a remarkable protective effect, and also was effective in counteracting the free radical toxicity by bringing about a significant decrease in peroxidative level. CONCLUSION: These recipes ameliorate liver damage induced by both ANIT and CCl4 despite the differences in their mechanisms of injury. Therefore they may be able to exert hepatoprotective effects through more than one mechanism of action because they contained a mixture of anti-hepatotoxic ingredients with mutual reinforcement and assistance.


Subject(s)
1-Naphthylisothiocyanate , Carbon Tetrachloride Poisoning , Chemical and Drug Induced Liver Injury/prevention & control , Drugs, Chinese Herbal/therapeutic use , Alanine Transaminase/blood , Animals , Aspartate Aminotransferases/blood , Chemical and Drug Induced Liver Injury/blood , Chemical and Drug Induced Liver Injury/etiology , Cholangitis/chemically induced , Cholangitis/prevention & control , Disease Models, Animal , Hyperbilirubinemia/chemically induced , Hyperbilirubinemia/prevention & control , Lipid Peroxidation/drug effects , Liver/metabolism , Liver/pathology , Male , Rats , Rats, Wistar
2.
Am J Chin Med ; 29(1): 155-60, 2001.
Article in English | MEDLINE | ID: mdl-11321473

ABSTRACT

The purpose of the study was to investigate the effects of two constituents of Panax notoginseng flower extract, Ginsenoside Rb2 and Rc, on human sperm motility and progression in vitro. Semen samples were collected from 20 patients with sperm motility between 20% and 40% of normal. All samples had sperm counts of over 20 million per milliliter, in accordance with the World Health Organization standard. Sperm were separated by a Percoll discontinuous gradient technique, and divided into a Percoll sperm control group, and three Ginsenoside Rb2 experimental groups (0.1, 0.01 and 0.001 mg/ml) and three Ginsenoside Rc experimental groups (0.1, 0.01 and 0.001 mg/ml). The results showed that at concentrations of 0.01 mg/ml and 0.001 mg/ml, Ginsenoside Rc enhanced both sperm motility and sperm progression significantly at the end of the 1st and 2nd hour. However, the three concentrations of Ginsenoside Rb2 did not increase sperm motility at the 1st or 2nd hour, but promoted sperm progression at the 2nd hour, when compared to the Percoll group.


Subject(s)
Ginsenosides , Panax , Plants, Medicinal , Saponins/pharmacology , Spermatozoa/drug effects , Adult , Humans , Male , Plant Extracts , Sperm Count , Sperm Motility/drug effects , Spermatozoa/physiology
3.
Am J Chin Med ; 29(1): 161-72, 2001.
Article in English | MEDLINE | ID: mdl-11321474

ABSTRACT

The inhibition ofarylamine N-acetyltransferase (NAT) activity by norcantharidin (NCTD), the demethylated form of cantharidin, in human hepatocellular carcinoma HepG2 cells was investigated. By using high performance liquid chromatography, NAT activity on acetylation of 2-aminofluorene (AF) and p-aminobenzoic acid (PABA) were examined. Two assay systems were performed, one with cellular cytosols, the other with intact HepG2 cell suspensions. The NAT activity in HepG2 cell line was inhibited by norcantharidin in a dose-dependent manner in both types of examined systems: i.e. the greater the concentration of norcantharidin in the reaction, the greater the inhibition of NAT activities. This report is the first to show that norcantharidin has an inhibitory effect on NAT activity in HepG2 cell.


Subject(s)
Antineoplastic Agents/pharmacology , Arylamine N-Acetyltransferase/antagonists & inhibitors , Bridged Bicyclo Compounds, Heterocyclic/pharmacology , Drugs, Chinese Herbal , Enzyme Inhibitors/pharmacology , 4-Aminobenzoic Acid/metabolism , Acetylation , Carcinogens/metabolism , Cell Survival/drug effects , Dose-Response Relationship, Drug , Fluorenes/metabolism , Humans , Kinetics , Substrate Specificity , Time Factors , Tumor Cells, Cultured
4.
Anticancer Res ; 17(3C): 2095-8, 1997.
Article in English | MEDLINE | ID: mdl-9216670

ABSTRACT

Norcantharidin[3], the demethylated product of cantharidin[1] has been used for the treatment of hepatoma, carcinomas of esophagus and gastric cardia, leukopenia and hepatitis. Since the enzyme xanthine oxidase is involved in the diseases mentioned above, and the reactive oxygen species produced by the enzyme induces DNA damage and oxidative damage of tissues, fourteen cantharidin analogues and cantharidimide derivatives were tested for their effects on xanthine oxidase. The results showed that these compounds, listed in Figure 1, displayed very weak inhibitory effects on xanthine oxidase. Contrary to expectation, disodium cantharidate [2], Norcantharidin [3], dehydronorcantharidin [4], disodium dehydronorcantharidate [5], N-(2-pyridyl) cantharidimide [12], N-(3pyridyl) cantharidimide [13] and N-(4-pyridyl) cantharidimide [14] showed a slight stimulating effect on xanthine oxidase at several concentrations.


Subject(s)
Cantharidin/analogs & derivatives , Cantharidin/pharmacology , Enzyme Inhibitors/pharmacology , Xanthine Oxidase/antagonists & inhibitors , Allopurinol/pharmacology , Antineoplastic Agents/pharmacology , Bridged Bicyclo Compounds, Heterocyclic/pharmacology , Cantharidin/chemistry , Kinetics , Molecular Structure , Structure-Activity Relationship
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