AIM To observe the effects of melatonin on acute and chronic injuries induced by oxygen and glucose deprivation (OGD) in co-cultured neuron and glia and to explore the probable mechanisms of melatonin in antagonizing the injuries. METHODS The injury model of cultured neuron and co-cultured neuron and glia was made by administration of sodium dithionite and glucose-deprived Earles solution. In neuron and glia co-culture, two different models, acute injury model at the phase of OGD and chronic injury model after 'reperfusion' were established. The levels of nitric oxide (NO) and the activity of lactate dehydrogenase (LDH) were measured by Griess reagent and LDH kits respectively. The content of malondialdehyde (MDA) was determined by TBA method. Cell viability was analyzed using colorimetric MTT assay. RESULTS Melatonin increased the level of NO at the concentration of 10 -6 , 10 -7 mol?L -1 and decreased the level of MDA content elevated by OGD at the concentration of 10 -6 , 10 -7 , 10 -8 mol?L -1 in vitro cultured cortical neurons. In the chronic injury model after 'reperfusion' melatonin (10 -6 , 10 -7 , 10 -8 mol?L -1 ) significantly decreased LDH activity and increased MTT value in neurons and glia co-cultured. But in the acute injury model, melatonin obviously increased LDH activity and decreased MTT value. CONCLUSION Melatonin protection for neuron from injuries induced by oxygen and glucose deprivation may be related to increase in the level of NO and decrease in the content of MDA. Melatonin can antagonize the injury in the chronic injury model after 'reperfusion', but exaggerate the injury in the acute injury model. These may be all related to its antioxidant action. Our results also suggest that melatonin may probably inhibit activation of microglia.

Object To investigate the therapeutic effects and mechanism of traditional Chinese compound decoction of Radix Curcumae (RC), Rhizoma Sparganii (RS), and Rhizoma Zedoariae (RZ) (DRRR) on liver fibrosis in rats induced by carbon tetrachloride (CCl 4). Methods Fifty Wistar rats were randomly divided into four groups: group A was healthy control (n=8), group B was model rats of liver fibrosis induced by CCl 4 (n=14), group C and D were treated with DRRR after the liver fibrosis in rats induced by CCl 4 four weeks later (n=14). B, C, and D groups were injected subcutaneously with CCl 4; C and D groups were administrated with DRRR 0.6 and 1.2 g/100 g, once per day. After administration of DRRR four weeks all rats were sacrificed, their blood and liver were harvested for further examination. The effect of DRRR was explored by the expressions and sites of transforming growth factor-beta 1 (TGF-? 1), Smad3 and Smad7 in liver tissues by immunohistochemical staining. The liver function, serum hyaluronic acid (HA), and liver histopathology were also examined by biochemsitry, RIA, HE, and Van Gieson stainings respectively. Results To compare with model group, in rats that received DRRR, the expressions of TGF-? 1 and Smad3 were significantly decreased, while the expression of Smad7 was obviously increased in the livers (P

Guan Xin Shu ( GXS ) is a heparinoid.Quails were randomly divided into 2 groups. All of them were fed with inducer diet containing 1% cholesterol and 20% fat for 6 weeks. 1 group was treated with GXS (200mg/kg/d, ip ) , the other with 0.9% NaCl(0.2ml/100g/d, ip ) . 4 and 6 weeks after administration, serum cholesterol level was significantly reduced (mean 3l%, P

Experimental research showed that Gan Tang Zhi can influence blood clotting and plasma fibrinolytic system of rabbits, 15min after introvenous injecting 6.25mg/kg or 25mg/kg Gan Tang Zhi into rabbit it can pronouncedly prolong prothrombin time ( PT ) , thrombin time ( TT ) , and kaolin partial thromboplastin time ( KPTT ) ; and cause remarkable increase of fibrin degradation product ( FDP ) , Gan Tang Zhi can also shorten englobulin lysis time (ELT) and decrease fibri-nogen.

The influences of propylene glycol mannate sulfate (PGMS) on experimental thrombosis and thrombolysis in vivo were studies after iv 8. 125, 6. 25, 12. 5 , 25mg/Kg in rabbits, and the effect of antithrombosis of PGMS was compared with that of heparin. The results showed that PGMS possessed remarkable effect of antithrombosis. In order to explore the mechanism of antithrombosis of PGMS, we studied the influences on the fibrinolytic and coagulant function of rabbits. The results showed that PGMS can pronouncedly prolong the prothrombin time (PT), thrombin time (TT), kaolin partial thromboplastin time (KPTT), and enhance the activity of antithrombin-III (AT -III). PGMS can cause a remarkable increase in fibrin degradation product (FDP) , shorten euglobulin lysis time (ELT) , and a decrease in the contents of fibrinogen and plasminogen activity. These results suggested that PGMS probably exert the antithrombotic effect by inhibiting coagulation and activating fibrinolysis.

The effects of eicosapentaenoic acid (EPA) on experimental thrombosis and its mechanism were studied. The results showed that eicosapentaenoic acid had a significant antithrombolic effect both in vivo and in vitro . EPA also had a fibrinolytic activity and can shorten euglobulin lysis time. Our studies also showed that EPA can inhibit platelet aggregation in rats. The plasma concentration of 6-keto-PGF1a and TXB2 was measured by radioimmunoassay. The results showed that EPA can reduce the contents of TXB2 and raise 6-keto-PGF1a/TXB2 ratio.

Objective To investigate the effect and its mechanism of “JinSanE” on liver fibrosis induced by carbon tetrachloride (CCl4) in rats. Methods Thirty-six Wistar rats were divided into three groups: healthy controls, CCl4 induced cirrhotic rats, and CCl4 induced cirrhotic rats treated with “JinSanE”, which was begun at the fourth week after exposure to CCl4. “JinSanE” was given once a day. Rats were killed after the administration of “JinSanE” for 4 weeks. The anti-fibrosis effect was determined by the expressions of connective tissue growth factor (CTGF) and transforming growth factor-? 1 (TGF-? 1) in liver tissue. The CTGF and TGF-? 1 mRNA expressions were detected by RT-PCR, CTGF and TGF-? 1 were assessed after immunohistochemistry staining. The serum level of hyaluronic acid (HA) was determined by RIA, and the liver histopathology was observed with light and electronic microscopy. Results Compared with the CCl4 induced cirrhotic rats, the expressions of TGF-? 1 and CTGF were decreased in the liver of the rats which were given “JinSanE” (P

Objective:To study the effects of WAK on immune function in mice.Methods: After different doses of WAK were given to mice ig, its effects on delayed type hypersensitivity (DTH), hemolysin production, NK and LAK cell killing activity were observed.Results: WAK could enhance DTH and hemolysin production in immunosuppressive mice and improve NK and LAK cell killing activity in mice.Conclusions: WAK could exhibit its antitumor effect by increasing immune function.

Objective: To study the protective effect of ginkgolide on rat's renal failure induced by adenine.Methods: The chronic renal functional failure model of rat was established with adenine. Its urea nitrogen (BUN), reatinine (Crea), Cholesterin (CH), total protein (TP), and albumin (ALP) in blood were determined. The pathologic changes were also observed. Results: Ginkgolide has effects on renal failure caused by adenine. Low and high dose groups decrease BUN. Crea, low dose group decrese CH, high dose group increase numbers of kindney glomerulus.Conclusion: Ginkgolide has protective effect on rat's renal failure induced by adenine.

Objective To investigate the effects of glycol mannate sulfate(GMS) on thrombogenesis.Methods The thrombogenesis was observed by carotid artery and cervical vein bypass and the thrombus was weighted.Thrombogenesis in common carotid artery was induced by electric stimulation.Mice mesentery microthrombus formation was induced by laser.Pulmonary thromboembolism was induced by injection of arachidonic acid.Plasma fibrinogen of rats was measured.Results GMS 25,50 mg?kg~(-1) could decrease the weight of thrombus cohered on suture silk significantly;25,12.5 mg?kg~(-1) of GMS could prolong the obstruction time;GMS 35.7,71.4 mg?kg~(-1) could delay the formation of mice mesentery microthrombus;GMS 40,80 mg?kg~(-1) could decrease the mortality induced by arachidonic acid injection.At the dosages of 25,50 and 100 mg?kg~(-1)GMS could decrease the fibrinogen in plasma.Conclusion GMS could inhibit the thrombogenesis significantly.