Yung-Luen Shih1,2,3, Jiann-Shang Chou4, Yung-Liang Chen5, Shu-Ching Hsueh6,7, Hsueh-Yu Chung8, Mei-Hui Lee9, Chao-Ping Chen1, Ming-Zhe Lee10, Hsin-Tu Hou10, Hsu-Feng Lu10, Kuo-Wei Chen11, Jing-Gung Chung12,13. 1. Department of Pathology and Laboratory Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan, R.O.C. 2. School of Medical Laboratory Science and Biotechnology, Taipei Medical University, Taipei, Taiwan, R.O.C. 3. School of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei, Taiwan, R.O.C. 4. Department of Anatomic Pathology, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C. 5. Department of Medical Laboratory Science and Biotechnology, Yuanpei University, Hsinchu, Taiwan, R.O.C. 6. Division of Hematology and Oncology, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C. 7. Family Medicine and Community Medicine, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C. 8. Jen-Teh Junior College of Medicine, Nursing and Management, Houlong, Taiwan, R.O.C. 9. Department of Genetic Counseling Center, Changhua Christian Hospital, Changhua, Taiwan, R.O.C. 10. Clinical Pathology, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C. 11. Division of Hematology and Oncology, Cheng Hsin General Hospital, Taipei, Taiwan, R.O.C. jgchung@mail.cmu.edu.tw ch1835@chgh.org.tw. 12. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C. jgchung@mail.cmu.edu.tw ch1835@chgh.org.tw. 13. Department of Biotechnology, Asia University, Taichung, Taiwan, R.O.C.
Abstract
BACKGROUND/AIM: Bufalin, bufadienolide present in Chan Su, has been shown to induce cancer cell apoptosis in many human cancer cells, including human leukemia cells, but its effects on immune responses are unknown. MATERIALS AND METHODS: This study investigated whether bufalin affected immune responses of mice with WEHI-3 cell-generated leukemia in vivo. BALB/c mice were intraperitoneally injected with WEHI-3 cells to develop leukemia and then were treated with oral treatment with bufalin at different doses (0, 0.1, 0.2 and 0.4 mg/kg) for 2 weeks. At the end of treatment, all mice were weighted and blood was collected; liver and spleen tissues were collected for cell marker, phagocytosis, natural killer (NK) cell activity and T- and B-cell proliferation measurements by using flow cytometric assays. RESULTS: When compared with the leukemia control group, bufalin increased the body weight, but reduced liver and spleen weights, and reduced CD3, CD16 and Mac-3 cell markers at 0.4 mg/kg treatment and increased CD11b marker at 0.1 and 0.2 mg/kg treatment. Furthermore, bufalin at 0.4 mg/kg increased phagocytosis by macrophages isolated from peripheral blood mononuclear cells and at 0.1 mg/kg by those from the peritoneal cavity. Bufalin (0.2 and 0.4 mg/kg) increased NK cell cytotoxic activity at effector:target ratio of 50:1. Bufalin increased B-cell proliferation at 0.1 and 0.2 mg/kg treatment but only increased T-cell proliferation at 0.1 mg/kg. Bufalin increased glutamate oxaloacetate transaminase level at all dose treatments, increased glutamic pyruvic transaminase level only at 0.1 mg/kg treatment, but reduced the level of lactate dehydrogenase at all dose levels in mice with WEHI-3 cell-induced leukemia in vivo. CONCLUSION: Bufalin increased immune responses by enhancing phagocytosis in mice with leukemia mice. Copyright
BACKGROUND/AIM: Bufalin, bufadienolide present in Chan Su, has been shown to induce cancer cell apoptosis in many humancancer cells, including humanleukemia cells, but its effects on immune responses are unknown. MATERIALS AND METHODS: This study investigated whether bufalin affected immune responses of mice with WEHI-3 cell-generated leukemia in vivo. BALB/c mice were intraperitoneally injected with WEHI-3 cells to develop leukemia and then were treated with oral treatment with bufalin at different doses (0, 0.1, 0.2 and 0.4 mg/kg) for 2 weeks. At the end of treatment, all mice were weighted and blood was collected; liver and spleen tissues were collected for cell marker, phagocytosis, natural killer (NK) cell activity and T- and B-cell proliferation measurements by using flow cytometric assays. RESULTS: When compared with the leukemia control group, bufalin increased the body weight, but reduced liver and spleen weights, and reduced CD3, CD16 and Mac-3 cell markers at 0.4 mg/kg treatment and increased CD11b marker at 0.1 and 0.2 mg/kg treatment. Furthermore, bufalin at 0.4 mg/kg increased phagocytosis by macrophages isolated from peripheral blood mononuclear cells and at 0.1 mg/kg by those from the peritoneal cavity. Bufalin (0.2 and 0.4 mg/kg) increased NK cell cytotoxic activity at effector:target ratio of 50:1. Bufalin increased B-cell proliferation at 0.1 and 0.2 mg/kg treatment but only increased T-cell proliferation at 0.1 mg/kg. Bufalin increased glutamate oxaloacetate transaminase level at all dose treatments, increased glutamic pyruvic transaminase level only at 0.1 mg/kg treatment, but reduced the level of lactate dehydrogenase at all dose levels in mice with WEHI-3 cell-induced leukemia in vivo. CONCLUSION:Bufalin increased immune responses by enhancing phagocytosis in mice with leukemiamice. Copyright
Authors: Aied M Alabsi; Rola Ali; Aini Ideris; Abdul Rahman Omar; Mohd Hair Bejo; Khatijah Yusoff; Abdul Manaf Ali Journal: Leuk Res Date: 2011-11-30 Impact factor: 3.156
Authors: James W Vardiman; Jüergen Thiele; Daniel A Arber; Richard D Brunning; Michael J Borowitz; Anna Porwit; Nancy Lee Harris; Michelle M Le Beau; Eva Hellström-Lindberg; Ayalew Tefferi; Clara D Bloomfield Journal: Blood Date: 2009-04-08 Impact factor: 22.113