ABSTRACT
Acute leukemia is one of the main causes of cancer in the world. Now a days using natural materials as source of anticancer drugs is more recommended. HESA-A is a drug of herbal-marine origin [patented by Iranian researcher]. HESA-A is composed of 50% inorganic substance? 45% organic substance [aminoenthraquinone] and 5% water. In this study effects of HESA-A? on NB4 cell line [Acute promyelocytic leukemia cells] was evaluated. HESA-A was prepared in normal saline as a stock solution [80 mg/ml, PH=7.4], and then was sterilized. After culturing and proliferation of NB4 cell line, the cells were treated by doses of 1, 2, 4 and 8 mg/ml of HESA-A. Respectively after 72h, the percentage of viable and dead cells were counted by using Trypan blue staining in Neubanr hemocytometer. Then by MTTassay, the percentage of cell survival were determined by ELISA reader in 570nm. Finally the effects of HESA-A on apoptosis were evaluated by flocytometery. This in vitro study shows that HESA-A has a cytotoxcic and antiprolifrative effects against NB4 cell line [Dose dependent].IC50 dose was 5mg/ml .HESA-A can result in apoptosis in 50% of the cells. Although the mechanism of HESA-A cytotoxicity action is not known, yet this study shows that this drug may cause apoptosis of cells by dose dependent method
ABSTRACT
Myocardial infarction [MI] is a major cause of morbidity and mortality worldwide. Epidemiological studies indicate that MI results from complex interactions between long-term environmental influences, concomitant disorders, and genetic susceptibility factors. Identification of genetic risk factors, particularly in premature MI, is very important. Since thrombosis plays a critical role in the pathophysiology of MI, recent studies focus on coagulation genetic polymorphisms. The critical role of platelets and their surface glycoproteins in the formation of occlusive thrombus leading to acute myocardial infarction is now well accepted. Platelets have two major receptors for collagen, glycoprotein I/IIa [integrin alpha [2] beta[1]] and glycoprotein VI. In the present study, platelet GP VI T13254C polymorphism was chosen due to its potential association with altered platelet reactivity. The aim of the present study was to determine whether or not GP VI T13254C polymorphism was associated with premature acute myocardial infarction. One hundred patients with premature acute myocardial infarction and 100 age-matched controls with normal coronary angiograms were studied. Genotyping was done using PCR followed by RFLP. Statistical analyses included chi-square, t-test and logistic regression model. The findings of the present study showed that the prevalence of T13254C polymorphism did not differ much between patient [38%] and control [33%] groups and that polymorphism was not associated with premature acute MI [P=0.46]. Logistic regression analysis also indicated no association between this polymorphism and premature acute MI [P=0.20]. This study showed that there was no significant association between GP VI T13254C polymorphism and premature acute MI