Ruscogenin Ameliorated Sjögren’s Syndrome by Inhibiting NLRP3 Inflammasome Activation

Figure 3

Ruscogenin inhibited the apoptosis of acinar cells in NOD/ShiLtJ mice and reversed TNF-α-induced apoptosis and inflammation of acinar cells. (a) Representative pictures of acinar cell apoptosis during AO/PI staining assay after the treatment of Ruscogenin. (b and c) Representative images of cell apoptosis (b) and apoptosis rates (c) were evaluated through flow cytometry assay after the treatment of TNF-α and Ruscogenin. (d and e) Representative images of protein bands (d) and relative protein expression of AQP5 and AQP4 (e) in acinar cells was tested by western blot after the treatment of TNF-α and Ruscogenin. GAPDH is a loading control. (f and g) Representative images of protein bands (f) and relative protein expression of NLRP3, caspase 1, and IL-1β (g) in acinar cells was assessed by western blot after the treatment of TNF-α and Ruscogenin. GAPDH is a loading control. vs. control group; ^∧p < 0.05, ^∧∧p < 0.01, ^∧∧∧p < 0.001 vs. TNF-α group. All experiments were repeated independently at least three times. Data were performed as the means ± standard deviation. TNF: tumor necrosis factor; AO/PI: acridine orange and propidium iodide; AQP: aquaporin; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; NLRP3: nucleotide binding oligomerization domain-like receptor 3; IL: interleukin.

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