Objective: To investigate the mechanism of Toll-like receptor in intestinal mucosal injury induced by infection in mice.
Methods: Totally 30 male BALB/c mice were randomly divided into a normal control group, 1week infection group and 2-week infection group. The mice of the 1-week and 2-week infection groups were sacrificed 7 days and 14 days after the infection respectively, and the mice of the normal control group were sacrificed 14 days after the infection. The model of intestinal infection of in mice was built by using the immunosuppressive method and oocyst intragastric administration. The pathological changes of the intestinal mucosa of mice were observed with a light microscope and the villus height, crypt depth and ratio of villus height/crypt depth were measured. The ultrastructure of the intestinal mucosa of mice was observed by a transmission electron microscope (TEM). The expressions of TLR2 and TLR4 in the intestinal mucosa were tested by qPCR and Western blotting.
Results: Under the light microscope, the intestinal villi were dropsical, obviously atrophied and shortened, and the submucosal structure was dropsical. The height of chorionic villi and the ratio of villus height to crypt depth in the jejunum of the 1-week and 2-week infection groups were significantly lower than those in the normal control group (all < 0.05), while the depth of the recess of the former two was significantly increased (all < 0.05). With the extension of the infection time, the villus height and the ratio of villus height to crypt depth in the jejunum of mice decreased significantly (both < 0.05), and the crypt depth increased significantly ( < 0.01). The TEM observation showed that the structure of the oocyst of in the jejunum of the infected mouse was intact, the villi around the oocyst were abscission seriously, and the oocyst wall was fused with the epithelial cell membrane. The qPCR observation showed that compared with the normal control group, the expressions of TLR2 mRNA and TLR4 mRNA in the intestinal mucosa of the 1-week and 2-week infection groups were significantly higher (all < 0.05). In addition, the expressions of TLR2 and TLR4 mRNA in the 2-week infection group were significantly higher than those in the 1-week infection group (both < 0.05). The Western blotting showed that the expressions of TLR2 protein and TLR4 protein in the intestinal mucosa of the 1-week and 2-week infection groups were significantly higher than those of the normal control group (all < 0.05). Furthermore, the expressions of TLR2 and TLR4 protein in the 2week infection group were significantly higher than those in the 1-week infection group (both < 0.05).
Conclusions: TLR2 and TLR4 are important receptors for intestinal mucosal recognition of . The infection may lead to intestinal mucosal damage possibly via the mechanisms associated with the up-regulation of TLR2 and TLR4 expressions.
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http://dx.doi.org/10.16250/j.32.1374.2018010 | DOI Listing |
Int J Pharm
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Drug Delivery and Disposition, KU Leuven, Gasthuisberg ON2, Herestraat 49 - box 921, 3000 Leuven, Belgium. Electronic address:
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View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
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School of Pharmaceutical Sciences, Zhejiang Chinese Medical University Hangzhou 311400, China.
To explore the mechanism by which vinegar-processed Euphorbiae Pekinensis Radix regulates gut microbiota and reduces intestinal toxicity, this study aimed to identify key microbial communities related to vinegar-induced detoxification and verify their functions. Using a derivatization method, the study measured the content of short-chain fatty acids(SCFAs) in feces before and after vinegar-processing of Euphorbiae Pekinensis Radix. Combined with the results of previous gut microbiota sequencing, correlation analysis was used to identify key microbial communities related to SCFAs content.
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