Fig. 2

Impact of PLGA incorporation on IL-1 ra biological activity. a Inhibition of interleukin-1 beta (IL-1β)-induced human lymphocyte proliferation by IL-1 ra or PLGA-encapsulated IL-1 ra (PLGA IL-1 ra). The percent inhibition of lymphocyte proliferation following treatment with 25 ng/ml of IL-1 ra or PLGA IL-1 ra was significantly higher than the percent inhibition of lymphocyte proliferation following treatment with 1 ng/ml of IL-1 ra or PLGA IL-1 ra. There was no significant difference in percent inhibition of lymphocyte proliferation between IL-1 ra and PLGA IL-1 ra treatments at 1 ng/ml or 25 ng/ml. *p < 0.001. Data represents the average ± SD of three independent experiments, each with duplicate wells per group. PLGA IL-1 ra was pooled from 4 different preparations. b cumulative sulfated glycosaminoglycan (sGAG) release, over 7 days, from control bovine articular cartilage explants (control), interleukin-1 α-stimulated (IL-1α), IL-1α stimulated + treatment with IL-1 ra at 20 ng/ml (IL-1 + IL-1 ra (20 ng/ml)), IL-1α stimulated + treatment with PLGA IL-1 ra at 20 ng/ml (IL-1 + PLGA IL-1 ra (20 ng/ml)), IL-1α stimulated + treatment with IL-1 ra at 100 ng/ml (IL-1 + IL-1 ra (100 ng/ml)) and IL-1α stimulated + treatment with PLGA IL-1 ra at 100 ng/ml (IL-1 + PLGA IL-1 ra (100 ng/ml)). (n = 6 in each group). IL-1α treatment resulted in a significantly higher sGAG cartilage release compared to control. Treatment with IL-1 ra or PLGA IL-1 ra at 20 ng/ml resulted in a significant reduction in sGAG release compared to IL-1α alone. Similarly, treatment with IL-1 ra or PLGA Il-1 ra at 100 ng/ml resulted in a significant reduction in sGAG release compared to IL-1 ra alone. There was no significant difference in sGAG release between IL-1 ra and PLGA IL-1 ra at 20 ng/ml or 100 ng/ml. *p < 0.001. Data represents the average ± SD of 6 explants per group. PLGA IL-1 ra was pooled from 4 different preparations