Figure 4.

Effect of various polyunsaturated fatty acids (PUFAs) on LXA4 secretion by RIN cells (rat insulinoma cells) treated with alloxan and streptozotocin. Alloxan and streptozotocin-induced inhibition of LXA4 secretion by RIN cells is restored to near normal by GLA, AA, EPA and DHA compared to control. (A) RIN5F cells were treated with various doses (1, 2, 4, 6 mM) of alloxan for 1, 2, 4 h. The LXA4 was estimated by ELISA in the supernatant of cultures. (B) RIN5F cells were treated with 10 μg/mL GLA, AA, EPA and DHA and alloxan (6 mM) for 1 h. Streptozotocin (21 mM) treated RIN cells (for 24 h) were exposed to 10 μg/mL of various PUFAs (C). The LXA4 was estimated in the supernatant of the cell cultures. * p < 0.05 compared to untreated control, # p < 0.05 compared to alloxan, compared to STZ. It is seen that at 10 μg/mL dose of EPA and DHA treatment there is no increase in LXA4 secretion by RIN5F cells in vitro in the presence of alloxan (6 mM) (Figure 4A). However, when RIN5F cells were supplemented with 15 μg/mL of EPA and DHA there is a significant increase LXA4 secretion even in the presence of alloxan (Figure 4B). In contrast 10 μg/mL of PUFAs could increase LXA4 secretion to near normal by RIN cells (Figure 4C) (AA > GLA > EPA > DHA). It is seen from this data that GLA, EPA and DHA can augment LXA4 formation but are less potent compared to AA. This suggests that some of the anti-inflammatory actions of GLA, EPA and DHA could be due to their action to enhance LXA4 formation in addition to their ability to give rise to PGE1 (from GLA); resolvins of E series from EPA and resolvins of D series, protectins and maresins from DHA. This data is taken from references [35,36].