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. 2023 Feb 16;12(4):636. doi: 10.3390/cells12040636

Figure 7.

Figure 7

MSC secretome administration prevented hepatic injury induced by AMI in an obese mouse model. Male mice were fed a high-fat diet (HFD) for 34 weeks and divided into three groups. During the last four weeks, one group did not receive additional treatment (HFD group), while a second group was treated daily with AMI (40 mg/kg) (HFD + AMI). The third group received MSC secretome endovenously once a week (HFD + AMI + secr). The microscopic evaluation of liver sections of obese mice treated with AMI revealed predominance of macrosteatosis, profound hepatocellular death with cytoplasmatic vacuolization, severe distortion of tissue architecture and multifocal inflammatory cellular foci. On the other hand, the coadministration of AMI with MSC secretome to obese animals resulted in great improvement of the histological appearance of the hepatic tissue, with predominance of microsteatosis and no evidence of inflammatory response. Additionally, a decrease in the number of infiltrating T lymphocytes macrophages cells in animals treated with AMI plus MSC secretome is observed. Representative micrographs of liver sections are shown. (a) Hematoxylin and eosin staining. The presence of inflammatory foci is indicated by arrows (scale bars represent 200 µm). Infiltration of T lymphocytes by (b) CD3 (Alexa 555, red) and (c) macrophages by F4/80 (Alexa 555, red) was evaluated by immunofluorescence. Nuclei were counterstained with DAPI (blue). Quantification of CD3 (e) and F4/80 (f) positive cells (arrows) was carried out by digital image analysis. The data are presented as means ± SEM of 30 random fields per animal and six animals per group. * p < 0.05 vs. control HFD mice; # p < 0.05 vs. HFD + AMI mice. To study the hepatic fibrosis, the immunoreactivity of α-SMA (d) was determined by confocal microscopy (Alexa 555, red) and the α-SMA mRNA levels (g) were measured by RT-qPCR. Alpha-SMA staining was almost completely absent from samples of untreated obese mice, however marked α-SMA immunoreactivity appear localized in perisinusoidal and pericellular areas of the livers from AMI-treated mice, while minimal staining was observed in animals treated with secretome. This result is in line with the hepatic level of α-SMA. Gene expression was normalized against GAPDH and expressed as fold of change vs. HFD-control group. Data are presented as means ± SEM (n = 4). * p < 0.05 vs. HFD-control group; # p < 0.05 vs. HFD + AMI.