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. 2023 May 8;13(9):2825–2842. doi: 10.7150/thno.81388

Figure 5.

Figure 5

NLRP3 deletion alleviates nicotine-induced atherogenesis and plaque vulnerability. (A) Serum IL-1β level in vehicle- or nicotine-infused Apoe-/- mice or Apoe-/-Nlrp3-/- mice. N=8. (B) Western blot analysis and quantification of inflammasome markers in aorta from vehicle- or nicotine-infused Apoe-/- or Apoe-/- Nlrp3-/- mice. N=4. (C) (Top) Representative images from BA lesions with Oil Red O staining and (Bottom) quantification of plaque size of BA in vehicle- or nicotine-infused Apoe-/- mice or Apoe-/- Nlrp3-/- mice. N=9. (D) (Top) Representative images and (Bottom) quantification of necrotic core area in the BA based on H&E staining of vehicle- or nicotine-infused Apoe-/- mice or Apoe-/- Nlrp3-/- mice. N=9. (E) (Top) Representative images and (Bottom) quantification of plaque collagen content in BA based on Masson trichrome staining of vehicle- or nicotine-infused Apoe-/- mice or Apoe-/- Nlrp3-/- mice. N=9. Scale bar: 100μm. Values are represented as mean ± SEM. *P<0.05 vs. Apoe-/- mice Veh. P<0.05 vs Apoe-/- mice Nic. Veh, vehicle; Nic, nicotine.