scholarly journals Pharmacological effect of indolicidin-like peptides on vasoactive substances content in experimental periodontitis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Igor V. Kutepov ◽  
◽  
Yuri D. Lyashev ◽  
Keyword(s):  
Pharmacological Effect ◽  
Vasoactive Substances ◽  
Experimental Periodontitis

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

Evaluation of a New Preparation of Urokinase

1973 ◽  
Vol 30 (01) ◽  
pp. 114-122
Author(s):  
C.R.M Prentice ◽  
K.M Rogers ◽  
G.P McNicol
Keyword(s):  
Body Weight ◽  
Maintenance Therapy ◽  
Initial Dose ◽  
Fibrinolytic Activity ◽  
Pharmacological Effect ◽  
Whole Body ◽  
Fibrinolytic Agent ◽  
Thromboplastic Activity

SummaryThe pharmacological effect of a new preparation of urokinase (Leo) has been studied, both in vitro and in six patients suffering from thrombo-embolic disorders. It was a non-toxic, effective fibrinolytic agent if given in sufficient dosage. A regimen consisting of an initial dose of 7,200 ploug units per kg body weight, followed by hourly maintenance therapy with 3,600 ploug units per kg intravenously, gave satisfactory evidence of whole body fibrinolytic activity. The preparation had minor but insignificant thromboplastic activity both when assayed in the laboratory and when given to patients.

Time course of serum levels of leukemia inhibitory factor (LIF) and soluble LIF receptor (sLIF-R) in development of stage II essential hypertension

2017 ◽  
pp. 63-69
Author(s):  
О.А. Радаева ◽  
А.С. Симбирцев
Keyword(s):  
Antihypertensive Therapy ◽  
Time Course ◽  
Pulse Wave ◽  
Antihypertensive Drugs ◽  
Peripheral Resistance ◽  
Serum Levels ◽  
Stage Ii ◽  
Healthy Individuals ◽  
Vasoactive Substances ◽  
Essential Arterial Hypertension

Цель - изучение сывороточных уровней LIF, sLIr и их соотношение с гемодинамическими параметрами (ЧСС, САД, ДАД, ПАД, ЦАД, срАД, УО, МОК, ОПСС, СПВ) и содержанием вазоактивных веществ (AT II, ET-1, NO, ADMA, SDMA, eNOS, iNOS, NT-proСNP, NT-proBNP) у пациентов с эссенциальной артериальной гипертензией (ЭАГ) II стадии. Методы: количество LIF, sLIF-R/gp190 и вазоактивные вещества в сыворотке определяли иммуноферментным методом. Результаты: у пациентов с ЭАГ II стадии вне зависимости от проведения гипотензивной терапии была более высокая концентрация LIF (7,54 (2,8) пг/мл, 7,5 (2,1) пг/мл), по сравнению с условно здоровыми - 1,25 (0,5) пг/мл, р<0,001. При этом у пациентов, не получавших гипотензивные препараты, увеличивался уровень sLIr - (5800 (1470 pg/ml)) по сравнению с больными на фоне гипотензивной терапии (4100 (1380) пг/мл, р<0,001) и условно здоровыми (3800 (1100) пг/мл, р<0,001). При уровне sLIF-R выше 4800 пг/мл обнаруживали связь с увеличением содержания в сыворотке iNOS, NT-proBNP, ADMA, SDMA, (r = 0,5-0,8, р<0,05-0,001) и уменьшением уровня eNOS (r = -0,56-0,86, р<0,05-0,001), что соответствует прогрессированию заболевания. Корреляции между LIF и указанными вазоактивными веществами выявлено не было, что дает основание предполагать, что sLIFr вызывает собственные патогенетические эффекты помимо антагонистической активности по отношению к LIF. Aim. To study levels of serum LIF and sLIF-R and their correlations with hemodynamic parameters (heart rate, systolic BP, diastolic BP, pulse pressure, central BP, mean BP, stroke volume, total peripheral resistance, and pulse wave velocity) and vasoactive substances (AT II, ET-1, NO, ADMA, SDMA, eNOS, iNOS, NT-proСNP, and NT-proBNP) in patients with stage II essential arterial hypertension (EAH). Methods. Serum levels of LIF and sLIF-R/gp190 were measured using ELISA in 180 patients with stage II ЕAН. Results: Patients with EAH II (with or without antihypertensive therapy) had higher serum levels of LIF (7.54 (2.8) pg/ml and 7.5 (2.1) pg/ml, respectively) compared to healthy individuals (1.25 (0.5) pg/ml), р<0.001. Patients not receiving a therapy had higher serum levels of sLIF-R (5800 (1470 pg/ml) than patients receiving antihypertensive drugs (4100 (1380) pg/ml, р<0.001) and healthy individual (3800 (1100) pg/ml, р<0.001). In patients with EAH, sLIF-R levels higher than 4800 pg/ml correlated with increases in iNOS, NT-proBNP, ADMA, and SDMA (r = 0.5-0.8, р<0.05-0.001) and decreases in eNOS (r = -0.56-0.86, р<0.05-0.001), which corresponded to disease progression. LIF did not show any significant correlations with these vasoactive substances, which suggested that sLIF-R exerted its own pathogenetic effects besides antagonizing LIF. Generally, this trend was typical for patients with EAH (II stage) without antihypertensive therapy.

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

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