Title : Inhibitory effect of berberine on interleukin-2 secretion from PHA-treated lymphocytic Jurkat cells.

Pub. Date : 2019 Jan

PMID : 30502647






5 Functional Relationships(s)
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1 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. Berberine mitogen-activated protein kinase 1 Homo sapiens
2 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. Berberine mitogen-activated protein kinase 1 Homo sapiens
3 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. Berberine mitogen-activated protein kinase 1 Homo sapiens
4 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. Berberine mitogen-activated protein kinase 1 Homo sapiens
5 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. Berberine mitogen-activated protein kinase 1 Homo sapiens