太子参化学成分、药理作用和应用的研究进展

太子参Pseudostellariae Radix是中国传统补益中药材之一,兼具药用和食疗功效,主要含有挥发油、多糖、环肽、生物碱、皂苷、酚类等成分,具有降血糖、抗炎、抗癌、保护细胞、抑制酪氨酸酶、免疫调节等药理作用。对太子参的化学成分及其药理作用,以及太子参在临床、食疗、保健食品、化妆品、兽药制剂和功能性饲料添加剂等方面应用进行总结,为太子参进一步开发利用提供依据。     

Selective Attention Effects on the Reflex Blink

Past work has shown that facilitation of reflex blinking accompanies cardiac deceleration when the attention of subjects is directed to a reflex-eliciting stimulus. The present studies showed that when warning stimuli directed attention instead to weak (tactile) stimuli presented simultaneously with reflex-eliciting (acoustic) stimuli, cardiac deceleration was still present but reflex magnitude was unchanged or inhibited. However, latency to reflex onset remained facilitated, i.e., latency and magnitude changes were discordant. The findings were interpreted as evidence for two independent processes: a process capable of selectively enhancing or attenuating sensory input and a non-selective process presumably facilitating motor pathways.     

The effect of an inhibitor of adenylate cyclase on the development of pyrogen,prostaglandin and cyclic AMP fevers in the rabbit

Summary An exotoxin of Bacillus thuringiensis known to inhibit adenylate cyclase in vitro has been used to investigate the role of cyclic AMP in the pathogenesis of fever in the rabbit. Intra-hypothalamic microinjections of the exotoxin are non-pyrogenic and significantly attenuate the hyperthermia caused by intrahypothalamic microinjections of both bacterial pyrogen (endotoxin) and prostaglandin E₁. The hyperthermia produced by dibutyryl cyclic AMP is not affected by the exotoxin. These results support the idea that adenylate cyclase is activated during the development of fever in the rabbit.     

Human Soluble Antigens and Their Use in Sperm Antibody Testing*

ABSTRACT: Efforts were made to disrupt and solubilize human sperm cells and to evaluate the product for its content of infertility antibody-related antigens. In the procedure that was developed, a well-washed sperm sample is treated with 0.1 M dithiothreitol for 60 min, followed by trypsin at 0.1 mg/ml for 30 min, and then by soybean trypsin inhibitor. A mixture of DNAses I and II are added. After centrifuging, the resuspended pellet (RP) and the final supernatant (FS) show several degrees of cellular breakdown. Immunological evaluation was done with a strongly positive human serum containing sperm-head antibody. From the inhibition of sperm agglutination, we could conclude that the desired soluble antigen was obtained in the FS fraction.     

Prejunctional inhibition of sympathetically evoked pupillary dilation in cats by activation of histamine H3 receptors

Summary Frequency-dependent pupillary dilations were evoked by electrical stimulation of the pre- or post-ganglionic cervical sympathetic nerve (sympatho-excitation) or the hypothalamus (parasympatho-inhibition) in sympathectomized anesthetized cats. Systemic administration of the selective histamine H₃ receptor agonist (R)--methylhistamine (RMeHA) produced a dose-dependent depression of mydriasis due to direct neural sympathetic activation but had no effect on responses elicited by parasympathetic withdrawal. The histamine H₂ receptor agonist, dimaprit, was inactive. RMeHA was much more effective in depressing sympathetic responses obtained at lower frequencies when compared to higher frequencies of stimulation.Responses evoked both pre- and postganglionically were inhibited by RMeHA. This peripheral sympathoinhibitory action of RMeHA was antagonized by the histamine H₃ receptor blocker thioperamide but not by intravenous pretreatment with the histamine H₁ receptor antagonist chlorpheniramine. Histamine H₂ receptor blockers cimetidine and ranitidine were also without effect. RMeHA did not depress pupillary responses elicited by i.v. (-)-adrenaline.The results demonstrate that histamine H₃ receptors modulate sympathetic activation of the iris at a site proximal to the iris dilator muscle. The predominant mechanism of action appears to the prejunctional inhibition of noradrenaline release from postganglionic sympathetic nerve endings. However, a concomitant ganglionic inhibitory action cannot be excluded. Correspondence to M. C. Koss at the above address     

Effects of 6-hydroxydopamine on pre- and post-junctional 5-HT1-like receptor-mediated responses in dog saphenous vein

Summary To investigate whether 5-HT₁-like receptor-mediated inhibition of adenosine 3 : 5-cyclic monophosphate (cyclic AMP) accumulation occurs in nerves or smooth muscle of saphenous vein, infusions of 6-hydroxydopamine (6-OHDA) were administered to dogs with the aim of inducing sympathetic nerve damage. The effects of 6-OHDA on other 5-HT₁-like receptor-mediated responses at the pre- and post-junctional level were investigated for comparison by studying 5-hydroxytryptamine (5-HT)-induced inhibition of ³H-noradrenaline release and contraction of smooth muscle respectively.Disruption of nerve function by 6-OHDA was revealed by the lack of catecholaminergic fluorescence and neurogenic contractile responses in saphenous veins from dogs treated with 6-OHDA. In addition, severe impairment of neuronal uptake mechanisms were apparent since basal efflux of ³H-noradrenaline, electrically-evoked release of ³H-noradrenaline and remaining ³H-noradrenaline content were considerably reduced. Some ³H-noradrenaline was taken up and released in 6-OHDA treated tissues which is consistent with the existence of nerve varicosities resistant to the present dosing regime of 6-OHDA, an observation substantiated by electron microscopy studies showing inconsistent lesions of nerve terminals.6-OHDA pre-treatment potentiated the smooth muscle contractile responses mediated by 5-HT₁-like receptors as well as potentiating 5-HT-evoked inhibition of prostaglandin E₂-stimulated cyclic AMP accumulation. It did not, however, affect 5-HT-induced inhibition of ³H-noradrenaline release. The present results suggest that inhibition of cyclic AMP accumulation by 5-HT occurs predominantly in smooth muscle. Correspondence to A. J. Kaumann at the above address     

Assessment of immunosuppression by serum inhibition of alloreaction and measurement of cyclosporin A (CyA) serum levels in kidney graft recipients under CyA

The immunosuppressive effect of kidney graft recipient sera was studied on T-lymphocyte alloreactive line (4H) proliferation and compared to native cyclosporin A (CyA) and CyA metabolite concentrations determined by radioimmunoassay (RIA) using specific or nonspecific monoclonal antibodies. Three clinical groups were studied: (1) patients experiencing acute renal rejection episodes (CyA-R), (2) patients experiencing CyA-dependent nephrotoxicity episodes (CyA-TOX) and (3) patients in a clinically steady state (CyA-ST), according to their therapeutic regimen i.e., monotherapy (CyA alone) or polytherapy (CyA associated with prednisolone and/or azathioprine). Regardless of the clinical state, sera of patients in polytherapy displayed more inhibitory activity than those of monotherapy patients (24% and 40% inhibition of 4H proliferation, respectively, at sera dilution of 1:2), something which was no doubt due to the inhibitory activity of prednisolone on T-lymphocyte growth. In the two therapeutic regimens, CyA-ST patient sera exhibited the lowest inhibitory activity on the 4H line (45% and 65% inhibition of 4H proliferation in mono-and polytherapy, respectively, at sera dilution of 1:2). Sera from CyA-TOX patients were highly inhibitory (74% and 86% inhibition of 4H proliferation in mono-and polytherapy, respectively, at sera dilution of 1:2), in agreement with RIA assays showing increased native circulating CyA and CyA metabolites and daily CyA intake in this group as compared to CyA-St. Surprisingly, CyA-R patient sera were no less inhibitory than those of CyA-ST patients on 4H-line, antigen-induced proliferation. This clinical group did not differ from others for CyA intake or level of circulating immunosuppressive molecules, suggesting that rejection could be associated with a state of interindividual variation in sensitivity to CyA. In addition, a polytherapeutic regimen seemed to modify CyA bioavailability in CyA-ST group patients, with a decreased CyA metabolite level as compared to their monotherapy counterparts (native CyA plus metabolite/native CyA ratio being 2.73 and 3.73, respectively). In contrast, in the CyA-R patient group, polytherapy appeared to be associated with an increase in CyA metabolite circulating levels (ratio 4.79). In view of the low inhibitory activity of CyA metabolites, this profile might lead to rejection.     

Epithelium-derived inhibition of [3H]acetylcholine release from the isolated guinea-pig trachea

Summary To investigate presynaptic, regulatory mechanisms on parasympathetic nerve fibres innervating the airways, the release of newly-synthesized [³H]acetylcholine from the isolated trachea was studied. Reverse phase HPLC followed by liquid scintillation spectrometry was used to separate and quantify the radioactive compounds choline, phosphorylcholine and acetylcholine in the incubation medium and the tissue.During the incubation of the tracheae with [³H]choline a significant synthesis of [³H]acetylcholine (35,000 dpm/preparation) and [³H]phosphorylcholine (500,000 dpm/preparation) occurred. In epithelium-deficient tracheae the formation of [³H]phosphorylcholine was enhanced, whereas the content of [³H]acetylcholine remained unchanged. The spontaneous outflow of tritium consisted mainly of [³H]phosphorylcholine (900 dpm/3 min) and [³H]choline (800 dpm/3 min); [³H]acetylcholine was only a minor fraction (50 dpm/3 min). Electrical stimulation of tracheae with intact epithelium caused only a small release of [³H]acetylcholine (460 dpm in the sample obtained during stimulation), but a considerable outflow of [³H]phosphorylcholine (1,900 dpm) without affecting the outflow of [³H]choline. Electrical stimulation of epithelium-deficient tracheae, however, induced a substantial release of [³H]acetylcholine (2,400 dpm), but only a small outflow of [³H]phosphorylcholine. Chemical stimulation (30 mol/1 veratridine) also caused a large release of [³H]acetylcholine (1,700 dpm) without affecting the outflow of [³H]phosphorylcholine or [³H]choline. Indomethacin (3 mol/1) enhanced the electrically-evoked release of [³H]acetylcholine from tracheae with intact epithelium by 89%.The present experiments demonstrate a strong inhibition by the epithelium of the electrically-evoked release of [³H]acetylcholine from the isolated guinea-pig trachea. Cyclooxygenase products of arachidonic acid do not appear as the main mediators of the epithelium-derived inhibition of acetylcholine release. Send offprint requests to I. Wessler at the above address     

“In vitro” and “ex vivo” effects of picotamide,a combined thromboxane A2-synthase inhibitor and -receptor antagonist,on human platelets

Summary Picotamide (G 137), a new non prostanoid inhibitor of in vitro arachidonic acid induced platelet aggregation, has been further characterized in in vitro and ex vivo studies.When whole blood was activated with collagen in the presence of picotamide 5×10^–4 M, thromboxane B₂ production was decreased, and 6-keto-PGF₁ generation was significantly increased, suggesting a reorientation of platelet endoperoxide metabolism following blockade of thromboxane synthetase. Picotamide also inhibited platelet aggregation and clot retraction induced by the endoperoxide analogue U46619 in human platelets, indicating thromboxane A₂-receptor antagonism, possibly of competitive nature.A single oral dose of picotamide 1 g in 24 healthy volunteers produced a significant inhibition of collagen, arachidonic acid and U46619-induced platelet aggregation. Serum levels of thromboxane B₂ were also reduced.Chronic administration of picotamide 1.2 g/d to patients with vascular disease resulted in a prompt and persistent fall in their increased plasma levels of -thromboglobulin.The results indicate that picotamide is a combined thromboxane B₂-synthetase inhibitor and thromboxane A₂-receptor antagonist in human platelets, and that it may prove useful as an antithrombotic agent.     

Age-related differences in sensitivity to organophosphorus pesticides

Organophosphorus (OP) pesticides are used extensively throughout the world to control undesirable pest species. The primary mechanism of action for OP insecticides is inhibition of acetylcholinesterase (AChE), an enzyme dynamically involved in cholinergic neurotransmission. Extensive inhibition of AChE leads to accumulation of acetylcholine in the synapse, disruption of normal impulse flow and subsequent signs of toxicity, including autonomic dysfunction, involuntary movements, muscle fasciculations and a host of others. It is generally believed that young individuals are more sensitive to the neurotoxic effects of these agents relative to adults. Essentially all studies addressing age-related differences in sensitivity to these toxicants have examined responses to acute exposures, however, using acute toxicity (lethality) as the endpoint. As the biochemical mechanism of toxicity for this class of toxicants (inhibition of AChE) is well known and considering that low level, repeated exposures are of great concern to the general public, we propose that evidence of neurochemical alterations, especially when exposures occur during development and maturation, is a more relevant endpoint of toxicity than lethality for estimating susceptibility. This report briefly summarizes previous and ongoing work in our laboratory which examines the relative sensitivity to these toxicants between young and adult rats.