Fig. 10
Representative photomicrographs of distal organs. Photomicrographs of slices from the liver (a–d), kidney (e–h), heart (i–l), spleen (m–p), and small bowel (q–t) stained with hematoxylin and eosin. a Normal liver architecture with intact hepatocytes (hep) surrounding the centrolobular vein (clv); b in the CLP-SAL group, liver damage was observed, with hepatocyte disarrangement (asterisk), hydropic degeneration of hepatocytes (single arrow), and an increased number of Kupffer cells (double arrows); c administration of nonpreconditioned AD-MSCs attenuated the liver architecture disarrangement (asterisk), hydropic degeneration of hepatocytes (single arrow), and number of Kupffer cells (double arrows); d administration of EPA-preconditioned AD-MSCs increased the number of regenerated hepatocytes (asterisk) and decreased the number of Kupffer cells (double arrows). e Normal kidney architecture with intact glomeruli (glo) and renal tubules (tub); f in the CLP-SAL group, kidney damage was characterized by acute tubular necrosis (single arrow) with glomerular damage (double arrows); g administration of nonpreconditioned AD-MSCs attenuated both the acute tubular necrosis (single arrow) and glomerular damage (double arrows); h administration of EPA-preconditioned AD-MSCs increased the number of regenerated renal tubules (asterisk) and further attenuated acute tubular necrosis (single arrow) and glomerular damage (double arrows). i Normal heart architecture with intact muscle fibers (mf); j in the CLP-SAL group, heart damage was observed, with interstitial edema (asterisk) and microvacuolization of muscle fibers (arrows); k administration of nonpreconditioned AD-MSCs attenuated the interstitial edema and microvacuolization (arrows); l administration of EPA-preconditioned AD-MSCs decreased the interstitial edema and restored muscle fibers (arrows). m Normal spleen architecture with white pulp (wp) and red pulp (rp); n in the CLP-SAL group, spleen damage was observed, with activation of lymphocytes in white pulp, increased number of megakaryocytes in red pulp (single arrows), and augmented number of lymphoblasts and lymphocytes in white pulp (double arrows); o administration of nonpreconditioned AD-MSCs maintained the activation of lymphocytes (double arrows) and decreased number of megakaryocytes in red pulp; p administration of EPA-preconditioned AD-MSCs decreased the reactivity of lymphoid follicles (double arrows) and the number of megakaryocytes in red pulp. q Normal architecture of small bowel with preserved villi (vil), lamina propria (asterisk), and crypt of Lieberkuhn (cry); r in the CLP-SAL group, small-bowel damage was observed, characterized by villi enlargement (single arrow), edema of lamina propria (asterisk), and increased number of enteroblasts in crypts of Lieberkuhn (double arrows); s administration of nonpreconditioned MSCs mitigated the villi enlargement (single arrow) and reduced number of enteroblasts in crypts of Lieberkuhn (double arrows); t administration of EPA-preconditioned AD-MSCs restored normal small bowel architecture mitigated edema of the lamina propria (asterisk) and led to a further reduction in the number of enteroblasts in crypts of Lieberkuhn (double arrows). Sepsis was induced by cecal ligation and puncture (CLP), while sham-operated animals were used as control (C). Twenty-four hours after surgery, the CLP group received saline (0.05 mL, SAL), adipose tissue-derived mesenchymal stromal cells (AD-MSC; 105 cells) (nonpreconditioned), or preconditioned with eicosapentaenoic acid (AD-MSC-EPA; 105 cells)