Catenarin Prevents Type 1 Diabetes in Nonobese Diabetic Mice via Inhibition of Leukocyte Migration Involving the MEK6/p38 and MEK7/JNK Pathways
Figure 1
Effect of anthraquinones on chemotaxis and cell viability (a). Chemical structure of 4 anthraquinones: catenarin, emodin, cascarin and rhein (b) and (c). JK-EF1α-CCR5 (b) and Jurkat cells (c) were incubated with the indicated doses (0–2.5 μg/mL) of catenarin (▲), emodin (●), cascarin (◆), rhein (▾), acetylsalicylic acid (x) or resveratrol (□), a negative control, for 1 h. The cells were subjected to chemotaxis assays in the presence or absence of MIP-1β (100 ng/mL) (b) and SDF-1β (100 ng/mL) (c) for 4 h. The migration index (MI) is presented as percentage (%). Data from 3 independent experiments are expressed as mean ± SE. P (*) < 0.05 (d). JK-EF1α-CCR5 cells (105 per well) were pretreated with the indicated doses (0–2.5 μg/mL) of resveratrol, acetylsalicylic acid, or the anthraquinones for 1 h; and cell viability was analyzed by WST-1 assay. Data from 3 independent experiments are presented as means ± SE. E. NOD splenocytes were preincubated with catenarin (1 μg/mL) or vehicle for 1 h. The cells underwent chemotaxis in the presence or absence of MIP-1α (100 ng/mL) and SDF-1β (100 ng/mL). Migration index (MI) was measured. Data from 3 independent experiments are expressed as mean ± SE. P (*) < 0.05. (f). Track plots showing the directional migration of Jurkat cells (left column) and JK-EF1α-CCR5 (right column) and, which were pretreated with vehicle (upper row) or catenarin (0.5 μg/mL, lower row), toward SDF-1β (50 ng/mL, left column) or MIP-1β (50 ng/mL, right column) in μ-slide migration assays. Each started in the center of the diagram with SDF-1β or MIP-1β on left side. Cells were tracked for 8 h. Tracks of cells moving toward and away from the chemokines are highlighted in black and red, respectively.
