Fig. 6: GPR35-mediated abnormal Trp metabolism sensing drives the repair of damaged-gut mucosa through KLF5.

A Schematic diagram of animal disposition process. B Representative images of rat colon tissues on day 10. C The changes of body weight (left panel) and DAS (right panel) of each group rats were monitored twice daily (n = 6–18). D Rat body weight and DAS of each group on day 10 (n = 18). E, F The relative body weight growth rate and DAS reduction rate during the period of day 10–17 (E) and 17–24 (F) were analyzed to characterize the change speed of rat body weight and DAS (n = 6–12). G, H Western blot analysis of ERK1/2 phosphorylation, PI3K/AKT pathway activation, KLF5 (G) and its mediated proliferation and migration related proteins (H) expression in the colon after rat administration on day 10. I HE and AB staining analyses of rat colon tissues, scale bars = 100 μm. J The relative variational amplitudes of inflammatory factor level in colon during the period of day 10–17 were analyzed to reflect the recovery speed of inflammation (n = 6). K The schematic form of proposed mechanism that GPR35 initiate and regulates damaged-gut mucosal repair through monitoring Trp metabolism (Created with BioRender.com, Agreement number: JO28T59X5V). Data are presented as means ± SD. Statistical analysis was performed using Student’s t test. *P < 0.05, **P < 0.01 and ***P < 0.001.