Protective Effect of Apigenin Against Vomitoxin-Induced Intestinal Injury in KM Mice
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Abstract:
Based on the intestinal damage in KM mice caused by deoxynivalenol (DON), The protective effects of apigenin (API) were investigated and its potential mechanisms were revealed in the study. Healthy male KM mice were randomly divided into a blank group, a DON group, a low-dose API group, a high-dose API group, a low-dose API intervention group (low-dose API+DON), and a high-dose API intervention group (high-dose API+DON). The protective effect of apigenin against vomitoxin-induced intestinal injury in KM mice was comprehensively assessed by weight monitoring of mice, pathological staining of colonic tissues with hematoxylin-eosin, TUNEL apoptosis staining, Western blotting apoptosis-related protein expression assay, and determination of serum lactate dehydrogenase (LDH), total superoxide dismutase (SOD), and malondialdehyde (MDA) content. The results of the study showed that the body weight of mice in the DON group decreased significantly after peaking on day 19 compared with the blank group, and the decreasing trend of body weight of mice was mitigated by the high-dose API intervention. Pathological examination revealed that colonic tissue damage was improved after high-dose API intervention, and the pathological score of damage was reduced by 1.3 compared with that of the DON group.TUNEL staining showed that the number of apoptotic cells was significantly reduced after API intervention, and Western blotting further confirmed that API intervention down-regulated the expression of apoptotic proteins Bax, P53, Caspase-12 and Caspase- 9 and decreased the expression of Bcl-2, and the expression of Bcl-2. 9 and decreased the expression of Bcl-2. Serological assays revealed that the high-dose API intervention reduced the LDH level by 7.5% (P<0.05), SOD activity by 46.8 % (P<0.05), and MDA content by 12.3% (P<0.05), compared with the DON group. Therefore, the above results indicate that API has a significant protective effect on DON-induced intestinal damage in KM mice, and its mechanism of action may be related to the inhibition of DON-induced apoptosis in colonic tissues, as well as the improvement of the synergistic multi-pathway effects such as serum LDH and SOD enzyme activities in mice. Strong theoretical support is provided for the potential application of apigenin as a functional food ingredient in the prevention and treatment of DON-related intestinal injury.
