scholarly journals Inhibitory Effect of Various Traditional Chinese Medicines on Rabbit Platelet Phospholipase A2 in Vitro and Suppressive Effect of Toki-syakuyaku-san on Increased Aggregability in Hypercholesterolemic Rabbit ex Vivo

1989 ◽  
Vol 109 (11) ◽  
pp. 869-876 ◽  
Author(s):  
Takashi SATO ◽  
Hiroyoshi YAMAGUCHI ◽  
Tetsuya FUJII ◽  
Satoshi AKIBA ◽  
Akira TAMURA ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Phospholipase A ◽  
Rabbit Platelet ◽  
Traditional Chinese Medicines ◽  
Chinese Medicines

ETHANOL INHIBITS RABBIT PLATELET RESPONSES TO COLLAGEN IN VITRO BUT DOES NOT AFFECT RABBIT PLATELET ADHERENCE TO DE-ENDOTHELIALIZED A0RTAE IN VIVO

1987 ◽  
Author(s):  
M L Rand ◽  
H M Groves ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
J F Mustard
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adherence ◽  
Induced Aggregation

Epidemiological studies indicate that moderate consumption of alcohol is associated with a reduced risk of coronary heart disease, but it is not known whether inhibition of platelet functions by ethanol is involved. We studied the effects of ethanol on rabbit platelet responses to collagen in vitro and in vivo. Addition of ethanol (4 mg/ml) to suspensions of washed platelets prelabelled with [14c]serotonin inhibited aggregation and secretion in response to low (0.4 μg/ml) concentrations of acid soluble collagen (14% secretion without ethanol, 3% secretion with ethanol). With a higher concentration of collagen (1.25 μg/ml), 4 mg/ml ethanol had no inhibitory effect. The inhibitory effect of ethanol on collagen-induced aggregation was also observed in citrated platelet-rich plasma (c-PRP) to which ethanol was added in vitro and in c-PRP from rabbits given ethanol acutely by gavage (3.5 g/kg) 30 min before blood sampling. The accumulation of [51cr]-labeled platelets on the subendothelium of rabbit aortae de-endothelialized with balloon catheters was measured in vivo in rabbits given ethanol (blood ethanol concentration at time of vessel wall injury: 4.1 ± 0.2 mg/ml, mean ± S.E., n=6). Ten min after de-endothelialization, there was no difference between the number of platelets adherent per square mm of injured aorta of control rabbits (39,400 ± 2,600, mean ± S.E., n=6) and intoxicated rabbits (36,800 ± 3,700, mean ± S.E., n=6). Thus, although ethanol inhibits platelet aggregation and secretion in response to collagen in vitro and ex vivo, it does not alter platelet adherence to the subendothelium, including its constituent collagen, in vivo. Therefore, it is unlikely that ethanol exerts its beneficial effects against coronary heart disease by altering the initial adherence of platelets to injured vessel walls.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Inhibition of Human and Animal Platelet Adhesiveness to Glass Bead Columns by Adenosine, Dipyridamole, Chlorpromazine and Acetylsalicylic Acid

1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu
Keyword(s):  
Guinea Pig ◽  
Acetylsalicylic Acid ◽  
Guinea Pigs ◽  
Glass Bead ◽  
Animal Species ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Platelet Adhesiveness

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.

Phenolic Acids Exert Anticholinesterase and Cognition-Improving Effects

2018 ◽  
Vol 15 (6) ◽  
pp. 531-543 ◽  
Author(s):  
Dominik Szwajgier ◽  
Ewa Baranowska-Wojcik ◽  
Kamila Borowiec
Keyword(s):  
Phenolic Acids ◽  
Ex Vivo ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
Amyloid Β Peptide ◽  
Beneficial Effects ◽  
Aβ Fibrils

Numerous authors have provided evidence regarding the beneficial effects of phenolic acids and their derivatives against Alzheimer's disease (AD). In this review, the role of phenolic acids as inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) is discussed, including the structure-activity relationship. In addition, the inhibitory effect of phenolic acids on the formation of amyloid β-peptide (Aβ) fibrils is presented. We also cover the in vitro, ex vivo, and in vivo studies concerning the prevention and treatment of the cognitive enhancement.

Biochemical and Pharmacological Properties of SANORG 34006, a Potent and Long-Acting Synthetic Pentasaccharide

Blood ◽  
1998 ◽  
Vol 91 (11) ◽  
pp. 4197-4205 ◽  
Author(s):  
J.M. Herbert ◽  
J.P. Hérault ◽  
A. Bernat ◽  
R.G.M. van Amsterdam ◽  
J.C. Lormeau ◽  
...  
Keyword(s):  
Thrombin Generation ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Factor Xa ◽  
Therapeutic Index ◽  
Inhibitory Effect ◽  
Experimental Models ◽  
Treatment And Prevention ◽  
Long Acting

Abstract SANORG 34006 is a new sulfated pentasaccharide obtained by chemical synthesis. It is an analog of the “synthetic pentasaccharide” (SR 90107/ ORG 31540) which represents the antithrombin (AT) binding site of heparin. SANORG 34006 showed a higher affinity to human AT than SR 90107/ORG 31540 (kd = 1.4 ± 0.3 v 48 ± 11 nmol/L), and it is a potent and selective catalyst of the inhibitory effect of AT on factor Xa (1,240 ± 15 anti–factor Xa U/mg v850 ± 27 anti-factor Xa U/mg for SR 90107/ORG 31540). In vitro, SANORG 34006 inhibited thrombin generation occurring via both the extrinsic and intrinsic pathway. After intravenous (IV) or subcutaneous (SC) administration to rabbits, SANORG 34006 displayed a long-lasting anti–factor Xa activity and inhibition of thrombin generation (TG) ex vivo. SANORG 34006 was slowly eliminated after IV or SC administration to rats, rabbits, and baboons, showed exceptionally long half-lives (between 9.2 hours in rats and 61.9 hours in baboons), and revealed an SC bioavailability near 100%. SANORG 34006 displayed antithrombotic activity by virtue of its potentiation of the anti–factor Xa activity of AT. It strongly inhibited thrombus formation in experimental models of thromboplastin/stasis-induced venous thrombosis in rats (IV) and rabbits (SC) (ED50values = 40.0 ± 3.4 and 105.0 ± 9.4 nmol/kg, respectively). The duration of its antithrombotic effects closely paralleled the ex vivo anti–factor Xa activity. SANORG 34006 enhanced rt-PA–induced thrombolysis and inhibited accretion of125I-fibrinogen onto a preformed thrombus in the rabbit jugular vein suggesting that concomitant use of SANORG 34006 during rt-PA therapy might be helpful in facilitating thrombolysis and preventing fibrin accretion onto the thrombus under lysis. Contrary to standard heparin, SANORG 34006 did not enhance bleeding in a rabbit ear incision model at a dose that equals 10 times the antithrombotic ED50 in this species and, therefore, exhibited a favorable therapeutic index. We suggest that SANORG 34006 is a promising compound in the treatment and prevention of various thrombotic diseases.

Bioinformatics-based Prediction of the mechanism and targets for BushenjieduDecoction in preventing relapse of acute leukemia

2020 ◽  
Author(s):  
Weilong Sun ◽  
Fujun Yang ◽  
Weipeng Shi ◽  
Xia Tao ◽  
Zhiwei Xi ◽  
...  
Keyword(s):  
Bioinformatics Analysis ◽  
Topological Analysis ◽  
Traditional Chinese Medicines ◽  
Potential Mechanism ◽  
Ppi Network ◽  
Chinese Medicines ◽  
Kegg Pathways ◽  
Long Time ◽  
Underlying Mechanisms

Abstract Background: Leukemia is a lethal myeloproliferative disorder, its’ relapse following chemotherapy is the major concern in clinical practice. For a long time, we found that traditional Chinese medicines such as Bushenjiedudecoction (BSJD) have significant effects on delaying relapse. However, the underlying mechanisms are not clear, which limits the clinical application of BSJD decoction. Methods: Therefore, we tried to make some explorations in this study. We isolated mesenchymal stem cells (MSC) after treated them with BSJD for proteomic analysis. And then 109 targets were screened out through analysis of the shared proteins of that affected by BSJD and those related to leukemia. Subsequently, the data were analyzed by GO functions, KEGG pathways, PPI network and topological analysis, and then some nodes were selected for animal experiment. Results: As a result, we demonstrated the effective targets of BSJD on MSC through bioinformatics analysis and explored the potential mechanism of BSJD from its influence on niches.These targets contains Hspb1、Dnmt1、Mmp2、Thbs1、Crebbp、Hmgb1、Acta2、Cdkn1b、Atg7、Tsc2 and Icam1. Afterwards, we confirmed BSJD reduced the gene expression of ICAM-1 through cultured MSC in vitro.Conclusions: We screened the potential targets of BSJD on MSC through proteomics and bioinformatics analysis, and selected some genes for experimental verification. These studies demonstrated the effect of BSJD on MSC. We hope that this research method could provide a new way of systematically studying the effects of traditional Chinese medicine on diseases.

scholarly journals Comparing the Effects of the mTOR Inhibitors Azithromycin and Rapamycin on In Vitro Expanded Regulatory T Cells

2019 ◽  
Vol 28 (12) ◽  
pp. 1603-1613 ◽  
Author(s):  
Marcus Bergström ◽  
Malin Müller ◽  
Marie Karlsson ◽  
Hanne Scholz ◽  
Nils Tore Vethe ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Ex Vivo ◽  
Mtor Inhibitors ◽  
Allogeneic Transplantation ◽  
Suppressive Effect ◽  
And Function ◽  
Treg Phenotype ◽  
Suppression Assay

Adoptive transfer of autologous polyclonal regulatory T cells (Tregs) is a promising option for reducing graft rejection in allogeneic transplantation. To gain therapeutic levels of Tregs there is a need to expand obtained cells ex vivo, usually in the presence of the mTOR inhibitor Rapamycin due to its ability to suppress proliferation of non-Treg T cells, thus promoting a purer Treg yield. Azithromycin is a bacteriostatic macrolide with mTOR inhibitory activity that has been shown to exert immunomodulatory effects on several types of immune cells. In this study we investigated the effects of Azithromycin, compared with Rapamycin, on Treg phenotype, growth, and function when expanding bulk, naïve, and memory Tregs. Furthermore, the intracellular concentration of Rapamycin in CD4+ T cells as well as in the culture medium was measured for up to 48 h after supplemented. Treg phenotype was assessed by flow cytometry and Treg function was measured as inhibition of responder T-cell expansion in a suppression assay. The concentration of Rapamycin was quantified with liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Azithromycin and Rapamycin both promoted a FoxP3-positive Treg phenotype in bulk Tregs, while Rapamycin also increased FoxP3 and FoxP3+Helios positivity in naïve and memory Tregs. Furthermore, Rapamycin inhibited the expansion of naïve Tregs, but also increased their suppressive effect. Rapamycin was quickly degraded in 37°C medium, yet was retained intracellularly. While both compounds may benefit expansion of FoxP3+ Tregs in vitro, further studies elucidating the effects of Azithromycin treatment on Tregs are needed to determine its potential use.

scholarly journals Arsenic Bioaccessibility of Realgar Influenced by the Other Traditional Chinese Medicines in Niuhuang Jiedu Tablet and the Roles of Gut Microbiota

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Wenfeng Xu ◽  
Shuo Xu ◽  
Shanshan Zhang ◽  
Xuejun Wu ◽  
Pengfei Jin
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Gut Microbiota ◽  
Incubation Medium ◽  
Toxic Elements ◽  
The Other ◽  
Traditional Chinese Medicines ◽  
Chinese Medicines ◽  
Scutellariae Radix

Niuhuang Jiedu tablet (NJT), a realgar (As2S2) containing Traditional Chinese Medicine (TCM), is a well-known formula. The safety of NJT is of growing concern since arsenic (As) is considered as one of the most toxic elements. NJT was demonstrated to be safer than realgar by our previous experiments and some other studies. The toxicity of realgar has been shown to be related to the amount of soluble or bioaccessible arsenic. In this study, the influences of the other TCMs in NJT on the bioaccessibility of arsenic from realgar, and the roles of gut microbiota during this process were investigated in vitro. Results showed that Dahuang (Rhei Radix et Rhizoma), Huangqin (Scutellariae Radix), Jiegeng (Platycodonis Radix), and Gancao (Glycyrrhizae Radix et Rhizoma) could significantly reduce the bioaccessibility of arsenic from realgar in artificial gastrointestinal fluids. Gut microbiota played an important role in decreasing the bioaccessibility of realgar because it was demonstrated to be able to absorb the soluble arsenic from realgar in the incubation medium. Dahuang, Huangqin, and Jiegeng could modulate the gut microbiota to enhance its arsenic absorption activity.

LEUKOCYTE MOTILITY: II. EFFECT OF ABSENCE OF GLUCOSE IN MEDIUM; EFFECT OF PRESENCE OF DEOXYGLUCOSE, DINITROPHENOL, PUROMYCIN, ACTINOMYCIN D, AND TRYPSIN ON THE RESPONSE TO CHEMOTACTIC SUBSTANCE; EFFECT OF SEGREGATION OF CELLS FROM CHEMOTACTIC SUBSTANCE

1967 ◽  
Vol 45 (2) ◽  
pp. 269-280 ◽  
Author(s):  
Bruce M. Carruthers
Keyword(s):  
Actinomycin D ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Medium Effect ◽  
Inhibitory Effects ◽  
In Vitro Motility ◽  
Directed Motility ◽  
A Minor ◽  
Chemotactic Effect

The random and directed motility of human leukocytes was studied in vitro. Motility was found not to be dependent upon glucose in the medium. 2-Deoxyglucose was found to inhibit all motility completely. Dinitrophenol had a minor suppressive effect on both random and directed motility. Puromycin at 10−3 M and actinomycin D at 10 μg/ml had a disproportionately great inhibitory effect on directed motility, when compared with minor inhibitory effects on random motility. Actinomycin D at 20 μg/ml and trypsin at 0.1 mg/ml were found to inhibit both types of motility almost completely. Segregation of starch from the field of leukocyte motility was found to abolish its chemotactic effect. Restoration of some chemotactic influence was seen if both starch and leukocytes were present in the segregated area.

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