Inhibitory effect of berberine on interleukin-2 secretion from PHA-treated lymphocytic Jurkat cells |
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| Affiliation: | 1. Aesthetic Medical Center, Department of Dermatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan, Republic of China;2. Department of Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan, Republic of China;3. Department of Physiology and Pharmacology, Chang Gung University, Taoyuan, Taiwan, Republic of China;4. Division of Endocrinology and Metabolism, Department of Internal Medicine, Chang Gung Memorial Hospital, Taoyuan, Taiwan, Republic of China;5. Department of Urology, Division of Geriatric Urology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan, Taiwan, Republic of China;6. Bioinformation Center, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan, Republic of China;7. Department of Nursing, National Quemoy University, Kinmen County, Taiwan, Republic of China;8. Division of Gastroenterology, Department of Internal Medicine, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan, Taiwan, Republic of China;9. Graduate Institute of Clinical Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan, Republic of China;10. Department of Nursing, Chang Gung University of Science and Technology, Taoyuan, Taiwan, Republic of China;11. Department of Nutrition and Health Sciences, Chang Gung University of Science and Technology, Taoyuan, Taiwan, Republic of China;12. Medical Center of Aging Research, China Medical University Hospital, Taichung, Taiwan, Republic of China;13. Department of Biotechnology, College of Health Science, Asia University, Taichung, Taiwan, Republic of China;14. Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan, Republic of China;1. Department of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, Saudi Arabia;2. Department of Clinical Laboratory Science, College of Applied Medical Science, University of Hail, Hail 2440, Saudi Arabia;3. Molecular Diagnostic and Personalised Therapeutics Unit, University of Hail, Hail 2440, Saudi Arabia;4. Interdisciplinary Biotechnology Unit, Aligarh, Muslim University, Aligarh, UP 202001, India;1. School of Human Development and Health, Faculty of Medicine, Institute of Developmental Sciences Building (MP887), University of Southampton, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK;2. Centre for Biological Science, Faculty of Natural and Environmental Sciences, University of Southampton, Southampton, UK;3. MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, UK |
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| Abstract: | Berberine is an isoquinoline alkaloid isolated from herb plants, such as Cortex phellodendri (Huangbai) and Rhizoma coptidis (Huanglian). Huanglian and Huangbai have been used as “heat-removing” agents. In addition, berberine has been reported to exert anti-inflammatory effect both in vivo and in vitro, where mitogen-activated protein kinase (MAPK) and cyclooxygenase-2 (COX-2) expressions are critically implicated. We herein tested the hypothesis that berberine exerts an anti-inflammatory effect through MAPK and COX-2 signaling pathway in T-cell acute lymphoblastic leukemia (T-ALL). In Jurkat cells, we found that PHA exposure caused elevation on interleukin-2 (IL-2) production in a time-dependent manner. PHA-stimulated reactions were steeply suppressed by berberine, such as IL-2 mRNA expression and protein secretion. However, berberine did not exert any cytotoxic effect at doses of 40 μg/ml. In addition, the possible molecular mechanism of anti-inflammation effect of berberine could be the inhibition of PHA-evoked phosphorylation of p38, since c-Jun N-terminal kinases (JNK) and extracellular signal-regulated kinase (ERK) expressions did not alter. Consistent with above results, berberine inhibition on PHA-induced IL-2 secretion could be reversed by treatment of SB203580, a specific inhibitor of p38-MAPK. Interestingly, upregulation of PHA-induced COX-2 expression was also observed following berberine treatment of Jurkat cells. Furthermore, flow cytometry analysis showed berberine-induced cell cycle arrest at G1 phase after PHA stimulation and decreased percentage of G2/M phase. In conclusion, our study demonstrated that the anti-inflammatory effect of berberine largely potentially results from its ability to attenuate p38 MAPK expression, and does not exclude a positive action of berberine on cell cycle arrest. These results provide an innovative medicine strategy to against or treat T-ALL patients. |
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