Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Figure 1 Magnolol prevents delayed small intestinal transit caused by LPS-induced sepsis. Data are shown as mean ± SE; n = 6. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^dP < 0.01 LPS/Mag vs LPS/Veh, LPS/Mag vs Control/Veh.

Figure 2 Change in spontaneous rhythmic contractions. A: Original traces of ileal circular muscle strip rhythmic contractions; B: Frequency of spontaneous rhythmic contractions. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^dP < 0.01 (LPS/Mag vs LPS/Veh) (n = 6).

Figure 3 The contractile responsiveness of circular muscle strips to betha-nechol. A: Bethanechol-stimulated dose-response curve; B: Circular muscle contractions at bethanechol concentration of 10 and 100 μmol/L. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^dP < 0.01 (LPS/Mag vs LPS/Veh) (n = 6).

Figure 4 RT-PCR analysis of (A) TNF-α, (B) IL-10, (C) MCP-1, and (D) iNOS mRNA expression in rat ileum. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^cP < 0.05 (LPS/Mag vs LPS/Veh) (n = 6); ^dP < 0.01 (LPS/Mag vs LPS/Veh).

Figure 5 NF-κB activity in rat intestine. A: Representative EMSA gel; B: Scanning densitometry analysis of NF-κB activity. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^cP < 0.05 (LPS/Mag vs LPS/Veh) (n = 3).

Figure 6 SOD activity (A) and MDA concentration (B) in rat ileum. ^bP < 0.01 (LPS/Veh vs Control/Veh); ^dP < 0.01 (LPS/Mag vs LPS/Veh) (n = 6).