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Showing 2 results for Hesa-A

Soodeh Namjoo, Fatemeh Nadali, Ahmad Kazemi, Hossein Dargahi, Hossein Rezaiezadeh, Shahrbanoo Rostami, Seyed Nasser Ostad,
Volume 6, Issue 3 (9-2012)
Abstract

Background and Aim: 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.

Materials and Methods: 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.

Results: This invitro 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.

Conclusion: 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.


Mahdihe Ghasemi, Fatemeh Nadali, Seyed Naser Ostad, Farhad Zaker, Shahrbanoo Rostamy, Hossein Dargahi,
Volume 6, Issue 4 (11-2012)
Abstract

Background and Aim: Chronic myelogenous leukemia is characterized by Philadelphia (Ph) chromosome, the presence of BCR-ABL fusion gene and constitutive activation of the ABL1 tyrosine kinase. Despite an excellent result of target therapy by imatinib, some patients develop resistance to imatinib. In this study Efficacy of HESA-A on proliferation and apoptosis of K562 cell line was assessed.

Materials and Methods: In this study doubling time of K562 cell line was calculated. The cells were affected by various concentrations of HESA-A(1,2,4 and 8 mg/ml respectively). Cytotoxicity and IC50 dose of HESA-A were detected by MTT and trypan blue exclusion assay. Apoptosis was assessed by flowcytometry after 48 h cell treatment in the presence of IC50 dose.

Results: Doubling time of K562 cells was 24 hours. HESA-A reduced the number of viable K562 cells in a concentration dependent manner.IC50 dose was 3.5 mg/ml. In flowcytometry analysis of apoptosis, 19.22% of the treated cells were located in the position of the necrotic cells.

Conclusion: The results of MTT and trypan blue exclusion assay suggest that HESA-A inhibits the growth of k562 cells in a concentration dependent manner and induces necrosis in K562 cells.



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