ASIA unversity:Item 310904400/111959
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    Title: Inhibitory effect of berberine on interleukin-2 secretion from PHA-treated lymphocytic Jurkat cells
    Authors: Hu, Sindy
    Hu, Sindy
    Ch, Chien-Wei
    Chen, Chien-Wei
    Chen, Szu-Tah
    Tsui, Ke-Hung
    Tan, Twen-Kei
    Tang, Twen-Kei
    Che, Hao-Tsai
    Cheng, Hao-Tsai
    Guey-Shyang
    Hwang, Guey-Shyang
    Yu, Ju-Wen
    Li, Yi-Chieh
    王錫崗
    Wang, Paulus S.
    Contributors: 生物科技學系
    Date: 2018-12
    Issue Date: 2019-09-10 05:17:47 (UTC+0)
    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.
    Relation: INTERNATIONAL IMMUNOPHARMACOLOGY
    Appears in Collections:[Department of Biotechnology] Journal Article

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