Objective To determine and compare the contents of total iridoids in valerian from different origins.Methods The total iridoids in valerian was detected by reaction with alkaline hydroxylamine-perchloric acid iron reagent,and the absorbance was measured at 522 nm by spectrophotometry. Results The content of valepotriate and its absorption were linear within the range of 0. 05-1. 40 mg·mL-1 . The average recovery was 98. 50%,and RSD was 1. 02%. There was significant difference between the contents of iridoid in valerian from different habitats. Conclusion This method is accurate and reliable for evaluating the quality of valerianand. The contents of valeriana is related to its habitats.

Objective To evaluate the effects and mechanism of valerian extract treatment on bleomycin-induced pulmonary fibrosis of rats. Methods After healthy Wistar rats(irrespective of sex)were given diethyl ether inhalation anesthesia, giving a single intratracheal instillation of bleomycin at a dose of 5 mg/kg to make a pattern of pulmonary fibrosis. 65 survival rats were randomly divided into four groups: Valerian high-dose groups(n = 16), Valerian low-dose groups(n = 16), Colchicine group(n = 16)and Model group (n = 17).Each group was given a dose of 100 mg/kg valeian extract everyday, a dose of 20 mg/kg valeian extract Valeian extract , a dose of 100μg/kg colchicine and a dose of 10ml/kg after second day. And in each groups, 6 rats were killed on day 7, 10 rats were killed on day 28 after instillation respectively. Rats in control group (n = 8) were instilled with saline intractracheally and saline was given everyday with a dose of 10ml/kg. Control group was killed on day 28. After rats were killed, The right lower pulmonary lobes were harvested for HE-staining, Masson-staining was used to observe the transformation of pulmonary tissue and immunohistochemistry was used to examine transforming growth factor-β1 (TGF-β1) which was analyzed by image analysis system. Results No obvious transformation were found in control group. The alveolitis in valerian and colchicine groups were ameliorated, compared with model group on day 7. The expressions of TGF-β1 in control group were lower than that in model group, and the mean integrated optical densities of TGF-β1 in control group were lower than that in mod-el group(P<0.05). The pulmonary fibrosis in valerian and colchicine group were ameliorated, compared with model group on day 28. The expressions of TGF-β1 in valerian and colchicine group were lower than that in model group. There were no significant differences between the valerian group and the colchicine group. Conclusion Valerian extract could reduce the degree of alveolitis and fibrosis induced by bleo-mycin through suppressing of TGF-β1.

BACKGROUND: In valerian-ligusticum extract (VLE), valeriana offici nalis extract (VOE) is γ aminobutyric acid (GABA) receptor kinetin, which can relax cerebral vascular spasm; ligusticum wallichii Fr. Extraxt (LWE)can pass through blood-brain barrier, enhance microcirculation of tissue and inhibit blood platelet aggregation and 5-Hydroxytryptamine (5-HT) release.OBJECTIVE: To probe into the effects of VLE prepared with effective components on prevention and treatment of cerebral ischemic injury.DESIGN:Complete randomized, negative and positive control experiment.SETTING: Institute of Senile Medicine and Pharmacology of Tongji Medical College of Huazhong University of Science and Technology.MATERIALS: The experiment was performed in Institute of Senile Medicine Pharmacology of Tongji Medical College of Huazhong University of ent blood perfusion in brain tissue: Fifty Kunming mice were employed,which was randomized into normal group, solvent control (model) group,ligustrazine 50 mg/kg group, VLE 170 mg/kg group and VLE 85 mg/kg Fifty Wistar rats were employed, which was randomized into solvent control (model) group, compound danshen (Radix Salviae Miltiorrhizae) 5 g/kg group,VLE 156 mg/kg group, VLE 94 mg/kg group and VLE 31.3 mg/kg group,Sixty Wistar rats were employed, which was randomized into sham-operation group, solvent control (model) group, ligustrazine 10 mg/kg group, VLE 156 mg/kg group, VLE 95 mg/kg group and VLE 31.3 mg/kg, 10 mice in each were employed, which was randomized into normal group, solvent control (model) group, ligustrazine 10 mg/kg group, VLE 200 mg/kg group and VLE 40 mg/kg, 10 mice in each one.sue, in advance, VLE (85, 170 mg/kg), ligustrazine (50 mg/kg) or solvent enhancer of equal volume (0.2 mL) were injected abdominally in each group. Twenty minutes later, pituitrin (2.5 u/kg) was injected intravenously; and 10 minutes later, isotope 99Tcm+ L, L-EthylCysteinate Dimer and Stannous Chloride (ECD) 3.7×1010Bq/ L(0.1 mL/per mouse) was injected in coccygeal nerve. Fifteen minutes later, radio-immunity counter was used periment of arteral-ovenous bypass method for thrombosis, before the opercal saline successively, continuously for 7 days, once per day. After 24 hours of medication pause, with abdominal anesthesia with pentobarbitol sodium, a catheter (with surgical thread inside) was used in vitro to connect common cervical vein and carotid artery. Thrombus mass was scaled 15 dominal anesthesia of chloral hydrate, intraluminal thread approach (ITA)was used to block unilateral MCA. Except that ITA was not used, the other management in sham-operation group was same as experimental groups.Gastric perfusion was done with VLE(156, 94, 31.3 mg/kg), ligustrazine operation and 3 hours and 12 hours after operation. 24 hours after modeling, the assessment was done for behavioral neurological damage and brain sive cerebral ischemia experiment, the model was prepared by coccygeal injection of collagen + adrenalin (AD). Respectively, 30 minutes before modeling injection and 1 hour after injection, gastric perfusion was done with VLE (200, 40 mg/kg), ligustrazine (10 mg/kg) or solvent enhancer of equal volume successively to observe the numbers of dead mice in 5 minutes after modeling and the numbers of hemiplegia mice in 15 minutes;and to determine brain mass index 8 hours later after sacrificed and lactic acid level of brain tissue homogenate with ultraviolet spectrophotometry.group.RESULTS: In the experiment of acute extensive brain ischemia in mice, in solvent control, during modeling, 3 mice were died and the rest 207 mice brain tissue in mice, the ratios of brain with and blood γ ray pulsating intensity in VLE 85 mg/kg group and VLE 170 mg/kg were higher than model group (0.53±0.09, 0.55±0.08, 0.45±0.08, t=2.234 6, 2.793 3, P method in rats, the thrombus masses in VLE 156 mg/kg group, 94 mg/kg group and 31.3 g/kg group were lower remarkably than the model group [(12.66±4.79), (13.31 ±3.97), (13.49±4.09), (19.21±5.76) g, (t=2.667 0,31.3 mg/kg group, 94 mg/kg group and 156 mg/kg group was lower remarkably than model group successively [(5.9±1.9), (6.0±2.0), (5.8±2.2),(8.7±0.9) score], and cerebral infarction index was lower than model group [(16.52±5.78)%,(16.54±3.00)%, (14.18±6.13)%, (24.03±4.85)%, (t=3.118 9-chemia in mice, brain mass indexes of VLE 40 mg/kg and 200 mg/kg groups were lower remarkably than model group [(0.91 ±0.20) and (0.82±0.24)%, (1.40±0.32)%], and lactic acid in brain tissue was lower than model group [(17.44±6.71),(14.43±2.81), (29.07±7.33) μmol/g (t=3.388 5-5.800 5, P＜ 0.01)].CONCLUSION: Valerian-liqusticum extract improves significantly cerebral ischemia in mice induced by pituitrin and the damage by medium cerebral artery embolism in rats, and it inhibits significantly blood platelet aggregation and thrombosis induced by AD+ collagen mixture or foreign objects. It is suggested that valerian-ligustrazine extract prevents and treats significantly the perfusion disturbance of cerebral microcirculation.

Objective To investigate the effect of morroniside on cycloxygenase (Cox) in the condition of platelet aggregation inducedby adenosine diphosphate (ADP) in rabbits. Methods The levels of Cox induced by ADP in different groups were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, all the morroniside groups significantly inhibited theincrease of Cox induced by ADP (P<0.001), which had concentration dependence, and the inhibition rate of high dose group was 30%. ConclusionMorroniside can decrease the level of Cox and it may be the mechanism of morroniside on inhibiting the platelet aggregation inducedby ADP in rabbits.