Objective: To probe into the antioxidation mechanism of lotus seedpod in vivo.Methods:Nineteen 4-month old rats were randomly divided into control group and procyanidins group. After feeding 100 mg/kg LSPC for 35 d, MDA and SOD in skin and serum, GSH-Px and Hyp in blood and skin were measured.Results: MDA levels in skin and serum in the procyanidins group were obviously lower than that of the control(P

Objective: To study the effects of procyanidins extract from the lotus seedpod (LSPC) on active oxygen radicals and lipid peroxidation. Methods: (1) The scavenging effects of LSPC on O ?- 2 and ?OH was investigated by using chemiluminescence method; (2) The effects of different concentrations of LSPC on RBC auto oxidation and LPO formation of rat liver mitochondria in vitro were observed; (3) The LPO level of liver homogenates incubated with Fe 2+ and H 2O 2 in vitro were determined; (4) the mice were treated with a single intragastric feeding of 5% CCl 4 soya bean oil solution (10ml/kg bw) after seven days supplementation of LSPC 100, 200, 400 mg/(kg bw?d). The activities of SOD, GST and the level of LPO in liver and plasma of CCl 4 toxic mice were determined. Results: In vitro, LSPC 169.0mg/L or 105.3mg/L was shown to markedly scavenge O ?- 2 produced in xanthine/xanthine oxidase and ?OH in Fenton systems respectively, and could significantly inhibit the formation of liver LPO. In vivo, LSPC (100,200mg/kg) evidently reduced the level of LPO and increase the activities of SOD and GST. Conclusion: It suggests that LSPC may be used as an antioxidant and might effectively protect liver from the injury due to lipid peroxidation.

Objective:To study the anti-tumor activity of ginkgo albumin (GA) and its mechanism. Method: Molecular weight of GAⅡa was detected by MS (mass spectrum). The antioxidative effect of GA was studied by deoxyribonucleic acid method and nitroblue tetrazolium (NBT) photo-reduction, and the anti-tumor activity of GA on S180 sarcoma was studied both in vivo and in vitro. Results: Molecular weight of GAⅡa was 29 248u. GA had strong scavenging effect on superoxide radical and hydroxyl radical. The growth of S180 both in vitro and in vivo was inhibited significantly by GA. Conclusion: The anti-tumor activity of GA was probably related with its antioxidative effect.

AIM To investigate the inhibitory effects on the growth of SMMC 7721 human hepatocellular carcinoma cell line and its mechanism by theasinesin. METHODS MTT assay,colony formation test, 3H TdR, 3H Leu incorporation test, determination of the intracellular cAMP and cGMP level, in situ hybridization were used. RESULTS Theasinesin at 50 mg?L -1 could significantly inhibit the growth and colony formation of SMMC 7721 cells. Theasinesin could strongly inhibit DNA and protein synthesis and increase intracellular cAMP levels. C myc gene expression was significantly decreased and p53 gene increased strongly in a dose dependent manner. CONCLUSION Theasinesin demonstrates significant inhibitory effects on the growth of SMMC 7721 cells. Its mechanisms may involve the inhibition of DNA and protein synthesis ,the elevation of intracellular cAMP levels, inhibition of c myc gene expression and enhancement of p53 gene expression.

AIM To investigate the mechanism of the anticancer effect of theasinesin. METHODS MTT assay, electronic microscopy technique, DNA gel electrophoresis, flow cytometric analysis with Annexin V Fluos staining,RT PCR and immunocytochemistry were performed for apoptosis and its mechanism. RESULTS After HL 60 cells were treated with theasinesin, HL 60 cells were characterized by condensation of the nuclear chromatin, margination against the nuclear envelope, and apoptotic body formation with scanning and transmission electronic microscopy. A typical DNA ladder was detected by agarose gel electrophoresis of DNA extracted from HL 60 cells. Flow cytometric analysis of HL 60 cells by Annexin V Fluos and propidium iodide double staining demonstrated that theasinesin induced apoptosis had dose effect and time effect relationships, but treatment with high dose or long time would induce cell necrosis principally. RT PCR and immunocytochemistry indicated that bcl 2 gene was reduced strongly in HL 60 cells. CONCLUSION\ Theasinesin induces apoptosis in HL 60 cells. The mechanisms for antitumor activity of theasinesin may involve in induction of apoptosis in cancer cells.

AIM　To investigate the inhibitory effects on the growth of SMMC-7721 human hepatocellular carcinoma cell line and its mechanism by theasinesin. METHODS　MTT assay,colony formation test, 3H-TdR, 3H-Leu incorporation test, determination of the intracellular cAMP and cGMP level, in situ hybridization were used. RESULTS　Theasinesin at 50 mg*L-1 could significantly inhibit the growth and colony formation of SMMC-7721 cells. Theasinesin could strongly inhibit DNA and protein synthesis and increase intracellular cAMP levels. C-myc gene expression was significantly decreased and p53 gene increased strongly in a dose-dependent manner.CONCLUSION　Theasinesin demonstrates significant inhibitory effects on the growth of SMMC-7721 cells. Its mechanisms may involve the inhibition of DNA and protein synthesis ,the elevation of intracellular cAMP levels, inhibition of c-myc gene expression and enhancement of p53 gene expression.

Object To study the immunomodulatory effects of theasinesin (TS) on human peripheral blood mononuclear cells (PBMC) in vitro. Methods The proliferation response of lymphocytes and IL 2 production of human PBMC were detected by MTT method. IL 2R expression was determined by immunocytochemistry and indirect immunofluorescence. The intracellular cAMP level was assayed by radioimmunoassay. Results 50, 150, 500 ?g/mL TS could enhance phytagglutinin (PHA) induced human PBMC proliferation in a dose dependent manner. The IL 2 production and IL 2R expression of PHA activated PBMC were increased markedly under the presence of TS. TS also decreased cAMP level of PBMC and intensively weaken the cAMP upregulating effect of prostaglandin E 1 (PGE 1). Conclusion TS possesses a potential immunoenhancing effect which might be made by decreasing the cAMP level of PBMC, promoting IL 2 production and IL 2R expression.

Objective:To study the effects of LSPC on impairment of learning and memory in mice induced by scopolamine and alcohol,and its possible mechanism.Method:One hundred male Kun-Ming mice were randomly divided into 2 batches,50 in each.Each batch was then divided into 5 groups(n=10):control,model,LSPC of 22.5,45,90 mg/kg bw.Group 3-5 was treated with lotus seedpod procyanidins(LSPC,dissolved in normal saline,22.5,45,90 mg/kg bw)by ig.each day for 20 d,while group 1-2 was treated with ig.normal saline.The model of learning and memory impairment was established by ip.3 mg/kg bw scopolamine hydrobromide or ig.40% alcohol in 0.1 ml/10 g bw respectively.Then,effect of LSPC on learning and memory in mice were tested by Y-maze.As to the mice whose learning and memory ability was impaired by alcohol,their brains were dissected out after Y-maze experiment for detecting the level of MDA,the activity of SOD and MAO-B.Results:The learning and memory abilities of mice impaired by scopolamine were remarkably improved after22.5 and 90mg/kg bw LSPC treatment.In the alcohol experiment,the impairment was significantly improved after three different doses of LSPC administration.The level of MDA was reduced,the activity of SOD increased and the activity of MAO-B decreased in mice that learning and memory was impaired by alcohol.Conclusion:LSPC can improve learning and memory abilities of the mice impaired by alcohol and scopolamine,and the mechanism in alcohol experiment probably lay on its suppressive effect on MAO-B activity and protection of neurons from oxidative stress.

The progress is reviewed on the studies of procyanicdins biological and pharmacological activities in the past ten years, including antioxidant,protecting cardiovascular system,regulating immunocompetence, antiviral, anticancer, antiulcer and antidepressant,antimutagenic properties, etc.