Fig. 4: LPC plays a role in promoting efferocytosis by binding to its receptor G2A.

CLO was used for macrophage knockout in adAtp8b1 PRSS1^Tg mice treated with careulein. A Structural alterations, fibrosis, and the expression of CD206 and ARG1 were evaluated by H&E staining, Masson’s trichrome staining, and immunohistochemical staining, respectively, of pancreatic tissues from PRSS1^Tg mice treated with caerulein in the adAtp8b1 and macrophage knockout groups. B Quantitative expression of IL-1β, IL-6, and TNF-α in pancreatic tissues from caerulein-treated PRSS1^Tg mice. C The concentration of LPC in pancreatic tissues from caerulein-treated PRSS1^Tg mice was measured by LC–MS/MS. D α-SMA expression detected by immunofluorescence staining was used to analyze the degree of fibrosis from PRSS1^Tg mice treated with caerulein in the adAtp8b1 and macrophage knockout groups. The mean gray values were used to quantitatively analyze the degree of fibrosis. E The mRNA expression of CD206 and ARG1 in the pancreatic tissues from adAtp8b1-treated and untreated PRSS1^Tg CP mice was measured by RT-PCR. F Structural alterations, fibrosis, and the expression of CD206 and ARG1 were evaluated by H&E staining, Masson’s trichrome staining, and immunohistochemical staining, respectively, of pancreatic tissues from CP model mice treated with or without commendamide (a G2A agonist). The data are presented as the means ± SDs. ns no significant difference; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001. Scale bars = 100 µm.