Induction of heme oxygenase-1 by Ginkgo biloba extract but not its terpenoids partially mediated its protective effect against lysophosphatidylcholine-induced damage.

In this study, we examined whether Ginkgo Biloba Extract and its terpenoid constituents protect against oxidative stress through actions on heme oxygenase (HO) gene expression and activity. HO-1 and glutathione peroxidase (GPx) gene expressions were examined by reverse transcription polymerase chain reaction (RT-PCR) analysis, HO activity and GPx enzyme activity were analysed by spectrophotometric assay. Pretreatment of H9c2 myocytes with 100-500 microgml(-1)Ginkgo Biloba Extract caused induction of HO-1 gene expression and a significant increase in HO activity; 30 microgml(-1)ginkgolide B and 30 microgml(-1)bilobalide had little effect. Treatment with Ginkgo Biloba Extract for 24 h also significantly increased GPx gene expression and GPx enzyme activity. Pretreatment with Ginkgo Biloba Extract, ginkgolide B and bilobalide protected myocytes against lysophosphatidylcholine (LPC)-induced damage. The protective effect of Ginkgo Biloba Extract against LPC-induced damage was partially suppressed by a HO inhibitor, Zinc protoporphyrin-IX (ZnPP-IX), while ZnPP-IX did not suppress the protective effect of ginkgolide B or bilobalide. Furthermore, pretreatment with hemin, biliverdin or bilirubin reduced cytotoxicity induced by LPC. These results suggest that induction of HO-1 by Ginkgo Biloba Extract but not its terpenoid constituents may play a beneficial role in oxidative stress. The mechanism of Ginkgo Biloba Extract-induced HO-1 gene expression and the increase in HO activity may be related to alteration of intracellular glutathione levels.

Protective effects of Ginkgo biloba extract against lysophosphatidylcholine-induced vascular endothelial cell damage.

AIM: To study the protective effects of Ginkgo biloba extract (GbE) against endothelial cell damage induced by lysophosphatidylcholine (LPC). METHODS: The vasorelaxation response to acetylcholine (ACh) were investigated in the isolated rabbit thoracic aorta. Lipid peroxidation products were determined by measuring thiobarbituric acid reactive substance. RESULTS: GbE attenuated the inhibition of vasorelaxation response to ACh and prevented the LPC-induced increase of malondialdehyde (MDA) content both in thoracic aortae. GbE prevented the leakage of LDH and the increase of MDA content in cultured endothelial cells in a concentration-dependent manner. GbE also markedly increased epoprostenol level in cultured endothelial cells treated with LPC. CONCLUSION: GbE protected endothelial cells against LPC-induced damage due to reduction in lipid peroxidation and facilitation of synthesis and/or release of epoprostenol.

Effects of gypenosides on mouse splenic lymphocyte transformation and DNA polymerase II activity in vitro.

AIM: To study the effects of gypenosides (Gyp) on lymphocyte transformation and DNA polymerase II activity. METHODS: Lymphocyte transformation response was induced by concanavalin A and lipopolysaccharides respectively. The activity of DNA polymerase II and DNA synthesis were assayed with TTP and [3H]TdR incorporation respectively in mixed lymphocyte culture test. RESULTS: Gyp 2.5-20 mg L-1 enhanced splenic T- and B- cell transformation, increased the DNA synthesis and potentiated the activity of DNA polymerase II. However, Gyp > 40 mg L-1 showed contrary effects. CONCLUSION: Gyp regulated lymphocyte transformation and DNA synthesis by regulating DNA polymerase II activity.

[Therapy of cantharides extract for perennial allergic rhinitis and its effect on total IgE in serum].

The therapy of 10% Cantharides extract in treating 50 cases of perennial allergic rhinitis (PAR) was studied. The extract was plastered and blistered on Dazhui, Neiguan point. It was observed by nasal mucosa provocative test, cells in nasal secretion test and serum total IgE test. The results showed that its effective rate was 88%, the allergic nasal mucosa provocative test of treated group alleviated obviously after the treatment (P < 0.01), the number of eosinophil and basophil in nasal secretion decreased (P < 0.01, P < 0.05); and the serum total IgE also reduced significantly (P < 0.01).

[Preliminary study on pathophysiology of liver-qi deficiency syndrome].

The authors advocate a program for diagnosing Liver-Qi Deficiency Syndrome (LQDS) based on the TCM theory and clinical practice. Through investigation, LQDS was found to be widely existed as latent period or as external manifestation, which occupied 18.85% in Qi Deficiency Syndrome. The subjects were divided into four groups including normal group, Spleen-Qi Deficiency Syndrome (SQDS) group, LQDS with Liver diseases (LD) and LQDS with non-Liver diseases (NLD) group. In order to explore the essence, the simultaneous determinations were done on lactate dehydrogenase (LDH) and its isoenzyme, dopamine beta-hydroxylase (D beta H), trace element Zn and Cu, and other serological indexes such as GPT, TP, Alb, A/G, etc. The results were, the content of LDH and trace element Zn in both LQDS-NLD and SQDS were significantly lower than that of normal group. D beta H reflecting sympathetic nerve function in LQDS-NLD was significantly higher than that of both normal and SQDS group; comparing LQDS-LD and LQDS-NLD group, the content of GPT, LDH, LDH5 and trace element Cu in former was significantly higher than that of the latter, but the content of TP, Alb, A/G, D beta H and Zn in former was remarkably lower than that of the latter. In order to avoid confusion, in studying this syndrome, one should distinguish LD and NLD.

[Protective effects of Panax notoginseng saponins on experimental myocardial injury induced by ischemia and reperfusion in rat].

Effects of total saponins of Panax notoginseng (PNS) and purified ginsenosides Rb1 and Rg1 from PNS on myocardial injury induced by cardiac ischemia and reperfusion were studied with rat hearts in situ and in vitro. In pentobarbital-anesthetized rats, PNS pretreatment (100 and 200 mg/kg) provided significant reduction in myocardial infarct size after left descending coronary artery ligation (40 min) and reperfusion (120 min) in comparison with the control. PNS 12.5 and 25 mg/L, Rb1 10 mg/L, and Rg1 10 mg/L significantly decreased cardiac CPK release, attenuated myocardial Ca2+ accumulation, reduced malondialdehyde (MDA) production and prevented reduction of superoxide dismutase (SOD) activity in comparison with the control in perfused isolated rat hearts with global ischemia (40 min) and reperfusion (15 min). The results show that PNS, Rb1, and Rg1 prevent cardiac ischemia and the action is considered to be related to the inhibition of lipid peroxidation.

[Effects of Panax notoginseng saponins on cardiac action potentials and slow inward current].

The effects of total saponins of Panax notoginseng (PNS) on contraction force, normal and slow response action potentials and slow inward current of guinea pig papillary muscles were studied by intracellular microelectrodes and voltage clamp techniques. The contraction force was decreased and the APD20, APD90 of normal AP were shortened in the presence of PNS 1 mg/ml, while the RP, APA and Vmax remained unchanged. The APA of slow AP induced with high K+ was decreased to 85% of its normal value after 20 min of perfusion with PNS solution. Isi was decreased from a peak value of 9.8 +/- 2.0 to effects of PNS on slow affecting INa. The 6.9 +/- 3.6 microA without AP and Isi were reversed by increasing calcium concentration. The results indicate that PNS has a selective blocking effect on calcium channels.

Studies on antihepatitic drugs. Total synthesis of (+/-)schizandrin C and its analogs.

This paper reports the total synthesis of (+/-) schizandrin, C, namely 5,6,7,8-tetrahydro-1, 12-dimethoxy-2, 3, 10, 11-bismethylenedioxy-6, 7-cis-dimethyldibenzo (a, c) cyclooctene (12B), a new active SGPT lowering principle isolated from the Chinese medical plant Schizandra chinensis, and its 6, 7-trans-dimethyl isomer (16B). We also synthesized two more isomers, namely 5, 6, 7, 8-tetrahydro-3, 10-dimethoxy-1, 2, 11, 12-bismethylenedioxy-6, and 7-cis-(and trans-) dimethyldibenzo (a, c) cyclooctene (12A and 16A). The NMR, UV and mass spectra of these four isomers are discussed. IR (in chloroform), UV, NMR and MS of synthetic schizandrin C (12B) are identical with those of the natural compound.