Ruscogenin Ameliorated Sjögren’s Syndrome by Inhibiting NLRP3 Inflammasome Activation

Figure 4

NLRP3 reversed the repressive effect of Ruscogenin on TNF-α-induced inflammation and apoptosis of acinar cells. (a and b) Representative images of protein bands (a) and relative protein expression of NLRP3 in acinar cells was tested by western blot after the transfection of NLRP3 overexpression plasmid. GAPDH is a loading control. (c and d) Representative images of protein bands (c) and relative protein expression of NLRP3, caspase 1, and IL-1β (d) in acinar cells was assessed by western blot after the treatment of TNF-α and Ruscogenin as well as transfection of NLRP3 overexpression plasmid. GAPDH is a loading control. (e and f) Representative images of protein bands (e) and relative protein expression of Bax and Bcl-2 (f) in acinar cells was assessed by western blot after the treatment of TNF-α and Ruscogenin as well as transfection of NLRP3 overexpression plasmid. GAPDH is a loading control. ^††† vs. NC group; vs. Control group; ^∧∧∧ vs. TNF-α group; ^#, ^##, ^### vs. TNF-α+Ruscogenin 10 group. All experiments were repeated independently at least three times. Data were performed as the means ± standard deviation. NLRP3: nucleotide binding oligomerization domain-like receptor 3; TNF: tumor necrosis factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL: interleukin; NC: negative control for NLRP3 overexpression plasmid.

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