ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of 4 renin-angiotensin system's(RAS) regulators (losartan, telmisartan, aliskiren and angiotenisin) on the human leukemia HEL cell growth.</p><p><b>METHODS</b>The HEL cells were treated with losartan, telmisartan, aliskiren and Angiotensin-(1-7) (Ang-(1-7)) for 12 days, respectively. The cell proliferation was measured by CCK-8 kit, the cell cycle and apoptosis were measured by flow cytometry.</p><p><b>RESULTS</b>The 10mol/L Ang-(1-7) markedly inhibited the growth of HEL cells, blocked cells at G/Gphase and markedly increased the late apoptotic cells (P< 0.001). The 10mol/L losartan and telmisartan, 10mol/L aliskiren had no effects on the proliferation, cell cycle and apoptosis of HEL cells (P>0.05).</p><p><b>CONCLUSION</b>Ang-(1-7), one of renin-angiotensin system's regulators, can inhibit the growth of HEL cells and promote the cell apoptosis. Ang-(1-7) may be one potential therapeutic drug for polycythemia vera with JAK2 mutation.</p>
ABSTRACT
<p><b>OBJECTIVE</b>To observe the therapeutic efficacy of 131I-labeled granulocyte macrophage colony-stimulating factor (GM-SCF) in SCID mouse-acute myeloid leukemia model, and the relationship between dose and effect.</p><p><b>METHODS</b>SCID-mouse acute myeloid leukemia model was established by injecting HL-60 cells through tail vein. GM-CSF was labeled with 131I by the chloramines-T method. SCID mice were randomly divided into 6 groups. Groups I, II and III treatment groups were given 9.25 x 10(5), 22.20 x 10(5) and 37.00 x 10(5) Bq of 131I-GM-CSF, respectively. Group IV was given 131I. Group V was given blending of 131I and GM-CSF. Group VI was control. Changes of HL-60 cells in blood and marrow, as well as white blood cells, red blood cells and platelets in blood were detected. Survival time of the SCID mice was calculated.</p><p><b>RESULT</b>It was observed that WBC, HL-60 cells in blood and marrow were less in treatment groups than that in control groups, especially in groups II, III. After 2 weeks of treatment, BPC of II, III groups increased remarkably (P < 0.01). Survival time of the SCID mice was prolonged in treatment groups (P < 0.01), especially in group III, the longest survival time of 60 days.</p><p><b>CONCLUSION</b>131I-GM-CSF could increase leukemic SCID mice survival rate. The therapeutic efficacy of low dose and mediate dose of 131I-GM-CSF is dose-dependent. 131I-GM-CSF is an effective radiation immunity therapy for leukemic mice.</p>
Subject(s)
Animals , Female , Humans , Mice , Antineoplastic Agents , Therapeutic Uses , Dose-Response Relationship, Drug , Granulocyte-Macrophage Colony-Stimulating Factor , Therapeutic Uses , HL-60 Cells , Leukemia, Myeloid, Acute , Drug Therapy , Mice, SCID , Xenograft Model Antitumor AssaysABSTRACT
<p><b>OBJECTIVE</b>To investigate the biodistribution of 131I-GM-CSF in SCID mice bearing human AML in vivo.</p><p><b>METHODS</b>The xenograft model of human leukemia was established in SCID mice. In the leukemia mice, the biodistribution of 131I-GM-CSF produced by chlo amine-T method was studied.</p><p><b>RESULTS</b>(1)The inoculated HL-60 cells could grow in SCID mice, which developed leukemia after 4 weeks. (2) 131 I-GM-CSF was concentrated in spleen, bone marrow and tumor tissue of the mice. In spleen and bone marrow, 131 I-GM-CSF was uptaken to peak in 30 minutes after injection, the up taking rate was (442. 9+/-86. 4) % ID/g and (4283. 8+/-252. 8)% ID/g, respectively, and maintained on higher level in 24 hours. The injection of 131I resulted in an even distribution in the whole body.</p><p><b>CONCLUSIONS</b>131 I-GM-CSF is able to concentrate electively in spleen, bone marrow and organs infiltrated by leukemia cells. The biodistribution of 131I-GM-CSF in the leukemia mice is tissue specific.</p>