Berberine sulfate ( Ber ) sc prolonged the survival time of mice under the condition of closed normobaric hypoxia, but Ber ig did not. Ber sc antagonized the effects of decreasing the survival time of mice by ip isoprenaline or phentolamine under the condition of closed normobaric hypoxia, prolonged decapitation-induced gasping duration in mice, and prolonged the survival time in mice poisoned by KCN, NaNO2 or lidocaine. Ber ig prolonged decapitation-induced gasping duration and the survival time in mice poisoned by lidocaine, too. But the effects of Ber ig were not so potent as Ber sc. The antianoxic effects of Ber was shown to be decreasing O2 consumption of body and raising the ability of body to utilize O2 under the condition of hypoxia.

The pharmacologic action of Atractylodis Rhizoma and its effective constituents in digestive system includes mainly anti-ulcer activity,acceleration of gastric emptying,regulation of gastrointestinal propellant movement,antidiarrheat effect,choleretic effect,hepatoprotection,and promotion of digestive and absorptive function.Atractylodis Rhizoma decreases gastric acid secretion via blockade of H2-receptor,and inhibits overexpression of inflammatory cytokines in gastric tissues to produce anti-ulcer effect.Atractylodis Rhizoma increases gastric mucosal blood flow,and improves growth and reparation of gastric mucosa to produce anti-ulcer effect by blockade of 5-TH receptor,and elevating levels of gastrin and trefoil factor in serum and gastric tissues.Atractylodis Rhizoma accelerating gastric emptying and gastrointestinal propellant movement is relative to decreasing release of central corticotropin-releasing factor,and stimulating vagal nerve,and promoting secretion of gastrin and motilin,and inhibiting secretion of vasoactive intestinal peptide,and blocking 5-HT-3receptor,and increasing amount of interstitial cell of Cajal.

By increasing the release of Ca2+ from sarcoplasmic reticulum in cardiomyocytes,salidroside elevates myocardial contraction,and by up-regulation of sarcoplasmic reticulum Ca2+-ATPase expression,and down-regulation ofcalcineurin expression to promote Ca2+ return to sarcoplasmic reticulum,salidroside obstructs Ca2+ overload-induced myocardial injury,and improves heart function.Salidroside inhibits lipid peroxidation,and increases activities of enzymatic antioxidants in heart tissue,and inhibits expression of inflammatory cytokines,and mitochondrial permeability transition pore opening,thus blocks myocardial apoptosis,by anti-oxidation and anti-inflammation;salidroside improves myocardial ischemia by up-regulation of hypoxia-inducible factor and vascular endothelial growth factor expression to promote angiogenesis in ischemic myocardium;salidroside improves respiratory function of mitochondria in myocardium by stimulating PGC-1 αt-NRF-1/NRF-2 signaling pathway to produce finally cardioprotective effect.These effects of salidroside are thought that are major mechanism of antagonizing cardiac injury induced by hypoxia,ischemia,ischemic-reperfusion,exhaustive exercise,chemicals,and biologic toxin.

Anti-oxidation of ursolic acid and oleanolic acid antagonizes oxidative stress-induced lipid peroxidation,inflammatory injury,steatosis,and fibrosis in liver tissue.Ursolic acid and oleanolic acid could block static state hepatic stellate cells activation and proliferation,and promote active state hepatic stellate cells apoptosis,thus decrease expression of collagen,and increase decomposition of extracellular matrix,to produce the effect in prevention and treatment of hepatic fibrosis by obstruction of JAK2-STAT3 signal transduction to inhibit NOX activation.Ursolic acid and oleanolic acid induce expression of detoxification enzymes and effiux transporters to reduce serum levels of bile acids and bilirubin,and liver levels of bile acids in cholestatic animal,thus ameliorating cholestatic liver injury and fibrosis.Ursolic acid and oleanolic acid inhibit occurrence and development of hepatic steatosis via decreasing hyperlipidemia to inhibit lipid out of liver accumulating to liver,inhibiting hepatic lipid synthesis,and improving lipid metabolism.

OBJECTIVE:To study the analgesic,anti-inflammatory and anti-thrombotic effects of Rhizoma Cynanchi Stauntonii.METHODS:Experiments were carried out on conventional mouse models of inflammation and pain,and on a thrombotic model of using direct current continuously to stimulate the carotid artery on one side of the neck of anesthetic rat.RESULTS:Alcoholic extract of Rhizoma Cynanchi Stauntonii,in dosages of 5g herb/kg and 15g herb/kg ig,prolonged the latent period of tail flip response to hot water stimulation and reduced acetic acid-induced writhing frequency,and inhibited xylene-induced swelling of the ear and carrageenin-induced swelling of the planta.The extract,10g herb/kg ig,prolonged in vivo coagulative time and thrombotic time induced by electric stimulating artery in rats.CONCLUSION:Rhizoma Cynanchi Stauntonii has analgesic,anti-inflammatory and anti-thrombotic effects.

OBJECTIVE:To study the anti-thrombotic,choleretic and anti-ulcerous actions of Rhizoma Ligustici METHO_DS:Experiments were carried out on conventional models of choleresis and ulceration,and on a thrombotic model of using direct current continuously to stimulate the unilateral carotid artery of anesthetic rat RESULTS:Alcoholic extract of Rhizoma Ligustici 3g herb/kg and 10g herb/kg id or ig,increased choleresis and prolonged the time for arterial thrombosis induced by electric stimulation in rats,but did not prolonged coagulative time,PT and KPTT The extract 5g herb/kg and 15g herb/kg ig,inhibited the formation of gastric ulcers induced by water immersion,stress,HCl and indomethacin-alcohol in mice CONCLU_SION:Rhizoma Ligustici has anti-thrombotic choleretic and anti-ulcerous actions

In vitro and in vivo animal model experiments have found that salidroside has protective effect for various causes induced injuries in various neurons and brain tissue.Its mechanisms of neuroprotection are multiple:(1)Protecting neurons from apoptotic injury by resisting oxidative stress,preventing intracellular Ca2 + overload,inhibiting caspase-3 activation,and attenuating hypoxia-induced abnormal metabolism of amyloid precursor protein;(2)promoting directional differentiation of stem cells into neurons and inducing neuronal regeneration;(3)promoting erythropoietin stimulating erythroblasts to be differentiated into erythrocytes and decreasing cerebrovascular resistance,and improving cerebral hypoxia-ischemia.Salidroside is expected to be used in the prevention and treatment of cerebral ischemic and neurodegenerative diseases,such as cerebral infarction,Alzheimer's disease,Parkinson's disease,amyotrophic lateral sclerosis,and diabetic encephalopathy.

Oxypeucedanin (OP) 300 and 600mg/kg ig inhibited the increased permeability of intraperitoneal blood capillary induced by ip 0. 7% acetic acid in mice, xylene-induced swelling of mouse ear, retarded gastrointestinal propellant rate of charcoal ink in normal mice,and reduced the incidence and frequency of purging induced by castor oil or senna in mice. These actions were enhanced in a dose-dependent manner. It is suggested that the antidiarrheal effect of OP is relative to its restriction against inflamation and gastrointestinal propellant function.

Salidroside antagonizes hypoxia,H2O2,hyper-glucose,homocysteine,smoking,orweightlessness-induced endothelial cell injury,and antagonizes the proliferation of vascular smooth muscle cells and vascular adventitial fibroblasts induced by hypoxia,hyper-glucose,noradrenaline,platelet-derived growth factor,or angiotensin Ⅱ,thus produces vascular protection and improves vascular function.Salidroside plays a dual role of vasoconstriction and vasodilation in regulating resistant blood vessel.The vasodilatory effect of salidroside is endothelium-dependent and endothelium-independent.Salidroside antagonizes vascular contraction and injury induced by KCl,CaCl2,noradrenaline,phenylephrine,homocysteine,hyper-glucose,plateau hypoxia,H2O2,and chlorine.Salidroside relieves cerebral vasospasm induced by subarachnoid hemorrhage,and pulmonary hypertension and pulmonary arterial remodeling induced by hypoxia or monocrotaline in rat,attenuates several experimental atherosclerosis,and enhances plaque stability.

Salidroside antagonizes hypoxia,H2O2,hyper-glucose,homocysteine,smoking,orweightlessness-induced endothelial cell injury,and antagonizes the proliferation of vascular smooth muscle cells and vascular adventitial fibroblasts induced by hypoxia,hyper-glucose,noradrenaline,platelet-derived growth factor,or angiotensin Ⅱ,thus produces vascular protection and improves vascular function.Salidroside plays a dual role of vasoconstriction and vasodilation in regulating resistant blood vessel.The vasodilatory effect of salidroside is endothelium-dependent and endothelium-independent.Salidroside antagonizes vascular contraction and injury induced by KC1,CaC12,noradrenaline,phenylephrine,homocysteine,hyper-glucose,plateau hypoxia,H2O2,and chlorine.Salidroside relieves cerebral vasospasm induced by subarachnoid hemorrhage,and pulmonary hypertension and pulmonary arterial remodeling induced by hypoxia or monocrotaline in rat,attenuates several experimental atherosclerosis,and enhances plaque stability.