Abstract
Calcium (Ca2+) is a ubiquitous second messenger regulating a myriad of cellular processes including proliferation, gene expression, and apoptosis. Agents that can modulate Ca2+ homeostasis are being extensively explored as potential anti‐inflammatory agents. Ellagic acid (EA), a polyphenolic compound found in many fruits and plant extracts, has been known to possess anti‐inflammatory properties. EA is thought to modulate Ca2+ homeostasis by enhancing sarcoplasmic endoplasmic reticulum ATPase pump (SERCA) activity, however effects of EA on Ca2+ signaling is not clearly understood. In order to study this relationship, we measured changes in Ca2+ transients in Jurkat T‐cells pretreated with EA (0–60 μM, 12 h). EA‐treated Jurkat T‐cells were challenged with SERCA inhibitor, thasipargin (TG) (2 μM). The amplitude of TG‐induced Ca2+ transient in the EA‐treated cells was 30% lower than vehicle control cells. The depletion of ER‐stores signals activation of store‐operated Ca2+ entry (SOCE) channels, resulting in Ca2+ influx. EA‐pretreatment induced a concentration‐dependent attenuation in SOCE‐mediated Ca2+ influx in Jurkat T‐cells. EA pretreatment also resulted in disruption of puncta formation in HEK293 cells overexpressing ORAI1 channels. The expression of certain cytokines is directly dependent on SOCE mediated Ca2+ influx. We demonstrated that EA‐treatment resulted in a significant decrease in IL‐2 and INFγ expression. Taken together, these results indicate that the anti‐inflammatory effects of EA could be attributed to its ability to attenuate store operated Ca2+ influx.
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