PubMed Health⌕ Search

Biomedical subjects

Anwar Umar

Publications and source records attributed to Anwar Umar.

9 recordsLinked to original sources
PubMed2006

Effect of Armagnac fractions on human platelet aggregation in vitro and on rat arteriovenous shunt thrombosis in vivo probably not related only to polyphenols.

UNLABELLED: Previous studies showed that alcohol-free extracts of Armagnac, an oak cask aged spirit rich in polyphenols, inhibit human platelet function in vitro and in vivo, in an experimental rat arteriovenous shunt thrombosis model and in human healthy volunteers. To identify active compounds, we fractionated a freeze-dried extract of a 10-year-old Armagnac using successively chloroform, diethyl ether and ethyl acetate. The 4 resulting fractions were tested on in vitro human platelet aggregation induced by ADP and in vivo on arteriovenous shunt thrombosis after 10 days oral treatment in rats. Active components were found mainly in fractions 1 and 3: at the highest concentration (2.4 10(-2) g/l), in vitro ADP-induced aggregation was inhibited by 62.7+/-2.1% and 51.2+/-3.8% for F1 and F3, respectively, vs 18.9+/-2.4% and 13.9+/-0.4% for fractions 2 and 4 and 33.6+/-1.5% for the crude extract. There was a significant decrease in thrombus weight with the crude extract and all fractions tested after 10 days treatment with 2.5 mg/kg/day orally, greatest with fraction 1. Characterisation of phenol content showed that fraction 1, the most biologically active, was essentially devoid of ellagic acid and ellagitannins, the polyphenols initially thought responsible for the effect, whereas fraction 2 which was mostly inactive, was the richest in polyphenols. CONCLUSION: The antiplatelet and antithrombotic activity of Armagnac seems mostly unrelated to polyphenols.

Alcoholic Beverages↗
PubMed2006

Aqueous extracts of Ocimum basilicum L. (sweet basil) decrease platelet aggregation induced by ADP and thrombin in vitro and rats arterio--venous shunt thrombosis in vivo.

OBJECTIVE: To study the effects of aqueous extract of Ocimum basilicum L (OBL) on platelet aggregation and experimental thrombus. METHODS: Platelet aggregation induced by ADP (5 muM) and thrombin (4 UI), and thrombus weight in an arteriovenous thrombosis (AVT) model were tested after 2 weeks treatment with 15, 75 and 375 mg/kg OBL orally in rats, compared to 8.8 mg/kg/day aspirin. AVT was also tested 2 h after 75 mg/kg OBL orally, after 3 and 7 days treatment, and one, three and seven days after the end of a two-week treatment. Analysis was done by ANOVA followed by protected t-tests (Tukey). RESULTS: OBL (15, 75, 375 mg/Kg) dose-dependently inhibits platelet aggregation by ADP and thrombin, with 75 mg/kg/day having approximately the same effect as 8.8 mg/kg/day aspirin. ADP induced aggregation reached 45%, 28% and 18% for OBL, respectively, 15, 75, 375 mg/kg compared to 71% for control and 27% for aspirin (all p<0.01 except aspirin vs. OBL 75 mg/kg/day p=0.7). Thrombin-induced aggregation reached 33%, 22%, 21% for OBL, respectively, 15, 75, 375 mg/kg compared to 67% for control and 48% for aspirin (all p<0.01 except OBL 75 vs. OBL 375 mg/kg/day, p=1.0). Compared to a control thrombus weight of 48.1 mg (SD 4.9), thrombus weight was 29.4 (3.3), 19.0 (1.9) and 12.3 (1.7) after treatment for 2 weeks with 15, 75 and 375 mg/kg OBL, respectively, and 27.4 (5.3) after 8.8 mg/kg aspirin (all p<0.001 except aspirin vs. OBL 75 mg/kg/day p=1.0). Maximum effect of OBL was reached after one week's treatment. The effect subsided between 3 and 7 days. CONCLUSION: OBL possesses an inhibitory effect on platelet aggregation induced by ADP and thrombin, that is dose-dependent and results in an anti-thrombotic effect in vivo which develops progressively over 7 days and disappears over 3-7 days. The active ingredient now needs to be characterized.

Adenosine Diphosphate↗
PubMed2005

Effects of armagnac or vodka on platelet aggregation in healthy volunteers: a randomized controlled clinical trial.

BACKGROUND: Cardiovascular mortality is especially low in southwest France (the French Paradox). In previous experimental studies, we found that alcohol-free extracts of armagnac could inhibit human platelet function in vitro and experimental thrombosis in vivo. To test the possible relevance of these findings, we tested the effects of daily use of small quantities of armagnac against same alcohol strength, polyphenol-free vodka in healthy volunteers. METHOD: Randomized controlled trial comparing 5-year old armagnac (30 ml/day for 2 weeks) to same alcoholic strength vodka, in 20 healthy volunteers, on platelet aggregation induced by ADP, collagen, and thrombin, as well as bleeding time, partial thromboplastin time (pTT), and plasma lipids during and after consumption. Platelet testing was done blind. RESULTS: After 14 days, ADP-induced platelet aggregation was inhibited more in armagnac (-31+/-3.2% compared to pretreatment values, p<.01) than in vodka (-11.0+/-6.8%, NS) users (p<.05, armagnac vs. vodka). A rebound increase of aggregation was found 2 weeks later in vodka but not in armagnac users. The same pattern was found for thrombin-induced aggregation, including post-treatment rebound. No effect was found on collagen-induced aggregation, bleeding time, pTT, or plasma lipids. CONCLUSION: The chronic ingestion of moderate quantities of armagnac modified platelet aggregation to ADP in healthy volunteers. The difference with the effects of same alcohol degree vodka is in favour of an effect of the nonalcoholic fraction in the effects of armagnac, rather than just alcohol. All spirits may not be equal for cardioprotection.

Adenosine Diphosphate↗
PubMed2005

Cytotoxicity of abnormal Savda Munziq aqueous extract in human hepatoma (HepG2) cells.

Abnormal Savda Munziq (ASMq) is a traditional Uighur medicinal herbal preparation commonly used to treat diseases such as diabetes, cardiovascular diseases, chronic asthma and especially digestive cancer. Earlier studies have shown that ASMq is a free radical scavenger and could prevent mitochondrial and DNA oxidative damage. In this study, we tested the effects of aqueous extract of ASMq on human hepatoma cells (HepG2) to explore the possible mechanism of its putative anticancer properties. Aqueous extract of ASMq was tested on HepG2 proliferation (MTT assay) at 72 h, cell viability at 48 h (neutral red assay), lactate dehydrogenase release over 48 or 72 h as a measure of cytoplasmic leakage, lipid peroxidation (malondialdehyde-thiobarbituric acid adducts) at 48 h, and incorporation of [3H]-leucine, [3H]-thymidine and [3H]-uridine into cellular protein, DNA and RNA, respectively, at 24 or 48 h to assess the inhibition effects to cellular macromolecule synthesis. Our results showed a significant (P < 0.05) time- and concentration-dependent inhibition of HepG2 proliferation and viability, with increased cytoplasmic leakage, and time- and concentration-dependent inhibition of protein, DNA and RNA synthesis. No lipid peroxidation was found at these concentrations. The results of the present study suggest that the putative anticancer mechanisms of ASMq may at least involve cytotoxicity.

Antineoplastic Agents, Phytogenic↗
PubMed2004

Protective effects of Munziq and Mushil of abnormal Savda to mitochondrial oxidative damage.

Munziq and Mushil of Abnormal Savda are traditional Uighur herbal medicinal products, which could have antioxidant properties protecting mitochondria against oxidative damage. Mitochondria were isolated from rat livers. A FeSO4/VitC hydroxyl radical-generating system was used to induce mitochondrial oxidative damage. Alterations in mitochondrial membrane structure were observed by electron microscopy, and mitochondrial superoxide dismutase (SOD) activity, malondialdehyde (MDA) level and Ca2+-Mg2+-ATPase activity were measured. Muziq or Mushil were added, at concentrations ranging from 10(-5) to 10(-1) g/mL. Mitochondrial membrane structure was damaged after exposure to hydroxyl radical; mitochondrial SOD and Ca2+-Mg2+-ATPase activities decreased (by 80 and 55%, respectively, both P < 0.01), and MDA level increased 4.6-fold (P < 0.01). Munziq and Mushil protected mitochondrial membranes from structural damage. They inhibited the changes in mitochondrial functions in a dose-dependent manner. At the highest concentrations, values were equal to initial normal values. Munziq and Mushil of Abnormal Savda can reduce the oxidative damage induced by hydroxyl radical and protect the mitochondrial membrane structure and its functions.

Animals↗
PubMed2004

Interactions between aspirin and COX-2 inhibitors or NSAIDs in a rat thrombosis model.

Recent in vitro studies, clinical trials and epidemiological studies have suggested possible interactions between aspirin and other cyclo-oxygenase (COX) inhibitors, such as ibuprofen of the COX-2 inhibitors celecoxib and rofecoxib. The objective of this study was to test the effects of aspirin (1, 2.5 and 5 mg/kg), and ibuprofen (4 and 15 mg/kg), diclofenac (2.5 mg/kg), flurbiprofen (2 mg/kg), celecoxib (7.5 mg/kg), and rofecoxib (1 mg/kg), alone or combined on a rat model of arterial thrombosis. Drugs were given orally daily for 7 days, before insertion of an arterio-venous shunt thrombosis system, left in place for 15 min. Main parameter was thrombus weight. Five to 12 rats were used per experiment, and 35 controls overall. Aspirin inhibited thrombus formation in a dose-dependent manner. All NSAIDS given alone also inhibited thrombus formation to approximately the same level as aspirin 1 mg/kg/day. Ibuprofen, celecoxib and rofecoxib inhibited the effects of aspirin, but not diclofenac or flurbiprofen. The interactions with aspirin do not seem to affect all NSAIDs to equal levels. The clinical impact of this needs to be confirmed in adequately powered clinical trials or pharmaco-epidemiological studies.

Administration, Oral↗
PubMed2003

Effects of armagnac extracts on human platelet function in vitro and on rat arteriovenous shunt thrombosis in vivo.

INTRODUCTION: The "French paradox", a low cardiovascular mortality compared to the prevalent risk factors, has been attributed to the regular use of red wine, and to the polyphenols it contains. These have among other effects an antioxidant and antithrombotic effect. The French paradox is maximal in southwest France, a region which is the region of production of armagnac, an oak cask aged spirit also rich in polyphenols. METHOD: We tested the effects of a freeze-dried extract of 12-year-old armagnac (EA88) on in vitro human platelet adhesion, and on aggregation induced by collagen or ADP, in the presence or absence of hypoxanthine-xanthine oxidase (HX/XO), at concentrations ranging from 5 x 10(-9) to 5 x 10(-3) g/l, after 15-60 min incubation. We also tested the effects of 2-week oral treatment with 1, 5 and 25 mg/kg EA88 in a rat arteriovenous shunt thrombosis model. RESULTS: EA88 inhibited ADP-induced but not collagen-induced human platelet aggregation in vitro in a concentration- and incubation time-dependent manner, which was greater in the presence of HX/XO. In vivo, giving rats a daily oral dose of EA88 for 2 weeks inhibited thrombus formation in a dose-dependent manner, for doses consistent with the habitual human use of armagnac. CONCLUSION: Armagnac extract EA88 had an antiplatelet and antithrombotic effect that if confirmed in man could contribute to explain the intensity of the French paradox in southwest France.

Adenosine Diphosphate↗
PubMed2003

Effect of age of Armagnac extract and duration of treatment on antithrombotic effects in a rat thrombosis model.

In a previous study, we had shown that freeze-dried extracts of 12-year-old Armagnac could inhibit ADP-induced platelet aggregation in a dose- and duration-dependent manner, and reduce thrombus weight in an experimental rat arteriovenous shunt thrombosis model after 2-week oral treatment. Polyphenol content could however vary with age and origin of the brandy, and the onset and offset of the effect were not defined. To this end, we studied the effects of extracts of 5-, 10- and 15-year-old Armagnac from two different producers at 1, 5 and 25 mg/kg orally for 15 days, on the same rat arteriovenous shunt thrombosis model. We then studied the effects of 1, 3, 7 and 15 days of oral treatment with 5 mg/kg extracts of a 5-year-old Armagnac, and the effect 1, 3 and 7 days after a 1-week oral treatment of the same extract at the same dose. There was a dose-dependent decrease in thrombus weight, which was similar for both Armagnac origins for all ages. Extracts of 5- and 10-year-old Armagnac were similar, and more potent than extracts from 15-year-old Armagnac. There was a progressive decrease in thrombus weight over duration of treatment to 7 days, to about 50% of initial thrombus weight. The effect disappeared within 3 days after stopping a 7-day treatment. We confirm the dose-, age- and duration-dependent inhibition of arteriovenous shunt thrombosis in vivo by Armagnac extracts in rats.

Administration, Oral↗