By the method of chemiluminescence, it was showed that BW-755C strongly inhibited the generation of active oxygen in PMNs stimulated by f-MLP, A23187 or opsonized zymosan A, while the inhibitory effect of indomethacin was quite weaker, Nifidipine, diltiazem and verapamil inhibited the generation of active oxygen in PMNs stimulated by A23187 at low concentration, but they did not block intracel-lular calcium ion increase stimulated by A23187. PGE1 was shown in to be a selective inhibitor of f-MLP-induced active oxygen production PMNs.

AIM: To study factors influencing mannitol to induce blood brain barrier (BBB) opening. METHODS: By constant flow pump, mannitol with different concentration (20% and 25%) was infused into left internal carotid artery of adult Wistar rats via their left external carotid artery at different speed and time. Firstly, after mannitol with a concentration of 25% was transfused, the optimal open time of BBB was investigated using Evans blue as an indicator by injection at different time (0, 2, 4, 6, and 8 min). Then influences of concentration of mannitol, speed of infusion, and change of time on mannitol to induce BBB opening were studied. Finally, death rate was counted according to sex and body weight in order to observe the influence of sex and body weight on tolerance of rats. RESULTS: The open degree of BBB was optimal after 2 min when 3.6 ml mannitol with a concentration of 25% was infused in 30 s at a speed of 0.12 ml?s -1 . However, mannitol with a concentration of 20 % did not almost have any effect on opening of BBB. Slowing of infusion speed or shortening of infusion time of mannitol reduced opening degree of BBB. Body weight affected rat tolerance to mannitol, and the tolerance of the rat was higher in those with higher weight. CONCLUSION: The factors influencing mannitol to induce BBB opening are as follows: concentration, infusion speed, and keeping time of mannitol. And the tolerance to mannitol is not concerned with the sex of the rats, but the body weight of the rats.

AIM: To investigate the protective effects and mechanisms of methylflavonolamine (MFA) on myocardial injury induced by adriamycin in mice. METHODS: The myocardial injury was induced by adriamycin (ADR) 1.5 mg?kg -1 ip once every two days for ten days in mice. All mice were taken the electrocardiogram examination before given drugs. The mice with abnormal electrocardiogram were excluded prior to the experiment. The degree of J point elevation, the prolonged degree of the QRS complex duration and the Q T interval, the change of contents of serum creatine phosphokinase (CK), serum lactate dehydrogenase (LDH), myocardial malondialdehyde (MDA), and the activity of myocardial superoxide dismutase (SOD) were observed in control and treated groups. The contents of serum CK and LDH were measured by spectrophotometry, and the content of myocardial MDA was measured by TBA method and the activity of myocardial SOD by hydroxylamine method. RESULTS: The J point was elevated, the Q T interval and the duration of QRS complex were prolonged and the contents of serum CK and LDH were increased in mice with acute myocardial injury induced by ADR, suggesting that a widespread and severe myocardial cell injury occurred in the prepared models. While all these injury indices were reversed by MFA treatment. The content of myocardial MDA was increased and the activity of myocardial SOD was decreased in mice with myocardial injury, and MFA decreased the MDA content and increased the SOD activity, indicating that it possesses the actions of scavenging free oxygen radicals and anti lipoperoxidation. CONCLUSIONS: MFA significantly alleviates the degree of the acute myocardial injury in mice induced by ADR. Its mechanism may be associated with reducing oxygen free radical production and anti lipoperoxidation.

Glycyrrhetic acid is a hydrolytic product of .glycyrrhizin which comes from Glycyrrhiza uralensis Fisch. This study showed that its sodium salt, sodium glycyrrhetinate ( SGA, 28mg/kg ip ) inhibited egg white or yeast-induced edema of rat hind paws; Meanwhile, SGA decreased prostaglandin E2 in inflammatory fluid. Malonyldialdehyde in mouse swelling paws stimulated by egg white was decreased by SGA and increased by arachidonic acid. The inhibitory action of SGA on production of malonyldialdehyde c.ould be entirely abolished by arachidonic acid,suggesting that phospholipase A2 bo inhibited by SGA. Also, SGA antagonized the contracting effect of inflammatory mediators such as histamine ( IC50 = 12 ,7mg/ L), 5 -hydroxytrypataminG (IC50=16.1 mg/L ) and SRS-A ( IC5O = 17.0mg/L)on isolated guinea-pig ileum. Because SGA inhibited cro-ton oil-induced ear-swelling of adrenalectomized mice, its anti-inflammatory action has no relationship with hypophysial-adrenocortial axis.

Effects of methylflavonolamine (MFA) on arachidonic acid(AA) metabolism pathway were studied. MFA (iv 40 mg ? kg-1) lightened the acute pulmonary thromboenblism signs in mice and reduced the mortality induced by AA. MFA(12. 5~200?mol ? L-1) in vitro dose-dependently inhibited rabbit platelet aggregation induced by AA. MFA(0.1~0. 4mmol ? L-1) in vitro dose - dependently inhibited rabbit platelet malondiadehyde(MDA) formation in-duced by AA. MFA(0. 4mmol?L-1) inhibited platelet MDA formation in rabbits induced by thrombin and AA. While propranolol inhibited MDA formation induced by thrombin but not by AA. MFA (0.4 mmol ? L-1) did not affect cAMP content in rabbit platelet. These results suggest that inhibitory effect of MFA on platelet AA metabolism may be one of the mechanism by which MFA inhibited platelet aggregation.

The effect of TRH on endotoxic shock in rats was studied, iv 0. 22-2 mg ?kg-1 TRH significantly reversed hypotension induced by iv coli E. endotoxin (40 mg ?kg-1) into rats and caused a 4. 2 kPa rise in mean arterial pressure (MAP). MAP after TRH administered could be stablized over a higher level than control for 30 min and maintained for 3 h during observation. Interestingly enough, the MAP rose gradually in TRH-treated rats as contrast with increasingly falling of that in control group during the late shock. TRH also improved 24 h sur-vival of shock rats. The dose-response relationship could be observed between 0. 22 ~0. 67 mg ?kg-1 TRH and disappeared over a highest dose (2 mg ?kg-1). It was shown that the best dose to reverse hypotension and to improve survival was 0. 67 mg ?kg-1 TRH. Naloxone 2 mg ?kg-1 showed the nearly same effect as 0. 22 mg ?kg-1 TRH in increasing MAP, but the former had higher 24 h survival of rats than the later.

Objective To evaluate the role of modified Buyanghuanwu decoction in the treatment of vascular dementia. Methods Adopting international standards for the diagnosis,30 cases with mild to moderate vascular dementia were treated by modified Buyanghuanwu decoction,six months as a course of treatment. 30 patients of the control group were treated by Yinxingye Tablets. Results After using modified Buyanghuanwu decoction,MMSE scores were increased (P

Objective To observe pre-syncopal limited tolerance and cardiovascular responses to head-up tilt combined with lower body negative pressure (HUT/LBNP) following exposure to head-down tilt (HDT, -1 Gz). Method Exposures to HUT/LBNP (-60 mmHg) in control session (without preceding 30 s -1 Gz treatment) and in simulated push-pull effect (PPE) session (with preceding 30 s -1 Gz treatment) were performed in 8 healthy adults. The changes of hemodynamic parameters were monitored by electrical impedance instrument during the experiments. Result The mean endurance time in presyncopal symptom limited HUT/LBNP in control session and in simulated PPE session were 8.4±2.1 min and 4.5±2.4 min, respectively, the two means were significantly different (P< 0.01). In simulated PPE session, as compared with baseline, heart rate (HR) during HDT was significantly lowered (P<0.01), while stroke volume (SV) and cardiac output (CO) were increased significantly (P<0.01). During HUT/LBNP, the increased percentage (relative to baseline) of HR in PPE session was lower than these in control session (P<0.05); the decreased percentages of SV and CO during HUT/LBNP in PPE session were both higher than those in control session (P<0.05). During HUT/LBNP, arterial pulse pressure (PP) of control session was significantly decreased than the value of baseline value (P<0.05); Total peripheral resistance (TPR) of PPE session was significantly increased than baseline value (P<0.05). Conclusion Tolerance time before the appearance of presyncopal symptoms during HUT/LBNP decreases and cardiovascular responses to HUT/LBNP are impaired, preceding exposure to HDT.

Plant polyphenols are a group of naturally occurring phytochemicals which are present in high amounts in plants and are the most abundant dietary antioxidants. Epidemiological and animal model researches have indicated that polyphenols can improve cognitive function. The mechanism for polyphenols to improve cognitive function has been extensively studied and may be owing to antioxidant, anti-imflammatory, neuroprotective, cerebrovascular blood flow increasing activities, and etc. Nowadays, the plant polyphenols and its benefits to cognitive function have become a hot research topic. In this article, we reviewed the latest progress from the structure and origin of phenolic compound, as well as its effect and action mechanism on cognitive function.

Aim To investigate the cytotoxic effect and mechanism of ampelopsin sodium ( AMP-Na ) on hu-man lung adenocarcinoma cell line GLC-82 alone or combined with carboplatin ( CBP ) . Methods The cytotoxic effect of human lung adenocarcinoma cell line GLC-82 was investigated by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide ( MTT ) colori-metric assay. Ultrastructure change of apoptotic GLC-82 cells was observed with transmission electron micro-scope. The changes of the cell apoptosis and the ex-pression of caspase-3 were analyzed with flow cytome-ter. Results Combined with AMP-Na, the IC50 of CBP decreased from (17. 10 ± 4. 78) mg·L-1 to <3. 12 mg·L-1(P<0. 01), showed that the combina-tion of AMP-Na and CBP had synergistic effect on GLC-82 cells ( CDI <1 ) . As with transmission elec-
tron microscope and flow cytometric analysis, the apop-tosis and necrosis ratios also increased in the combina-tion group. The necrosis ratios increased from (2. 56 ± 0. 41 )% to ( 71. 83 ± 5. 43 )% ( P<0. 01 ) . The ex-pression of caspase-3 was increased significantly after treated with AMP-Na or combined with CBP. Conclu-sions There is a synergistic cytotoxic effect on GLC-82 cells treated with AMP-Na combined with CBP. Ap-optotic cells and necrotic cells are found in GLC-82 cells treated with AMP-Na alone or combined with CBP. One of the mechanisms to induce apoptosis is probably that activation of caspase-3 mediates signal transduction pathway in cells.