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. Author manuscript; available in PMC: 2023 Jan 1.
Published in final edited form as: Pain. 2022 Jan 1;163(1):180–192. doi: 10.1097/j.pain.0000000000002330

Figure 7. β2AR regulated colonic inflammation, visceral hypersensitivity, and activity of SGCs of DRG.

Figure 7.

TNBS-induced colonic inflammation was characterized by macroscopic examination (A), H & E stain (B), analysis of colonic structures (C), and expression of pro-inflammatory factors in the colon (D). TNBS-induced visceral hypersensitivity was characterized by painful behavior in response to noxious CRD at 40 mmHg or 60 mmHg (E). TNBS-induced and β2AR-mediated SGC activity was characterized by the expression of GFAP (F). β2AR inhibitor also suppressed β2AR levels in DRG (F). The activity of β2AR was modulated by its agonist (Form) or antagonist (ICI). n>3. p<0.05 (*), 0.01 (**), or 0.001 (***).