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Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2016-Jun

[The preventive effect of total saponins of Panax japonicus on nonsteroidal anti-inflammatory drug-induced enteropathy].

Само регистровани корисници могу преводити чланке
Пријави се / Пријави се
Веза се чува у привремену меморију
Ying Mei
Zhaozhao Xiao
Jinwu Feng
Ting Wang
Changcheng Zhang
Ding Yuan
Chaoqi Liu

Кључне речи

Апстрактан

Objective To investigate the preventive effect of total saponins of Panax japonicus (SPJ) on nonsteroidal anti-inflammatory drug (NSAID)-induced intestinal injuries in mice. Methods NSAID-induced intestinal mucosal damaged models were established by intragastric administration of 5 mg/mL diclofenac sodium in mice for continuous 2 days. Since 4 days before the modeling, the mice in the experimental group were given SPJ once a day for 6 days. The small intestinal mucosal permeability was detected by fluorescein isothiocyanate-dextran (FITC-DT) and Evans blue staining. The small intestinal mucosal lesions were observed by HE staining; immunofluorescence staining was used to determine the expressions of endoplasmic reticulum stress response protein glucose transporter protein 78 (GRP78) and tumor necrosis factor alpha (TNF-α) in the intestinal mucosal epithelial cells. Results In the model group, small intestinal mucosal injury was serious. Evans blue staining and FITC-DT labeling showed the blue spots were denser and mucosal permeability increased significantly in the model group. HE staining revealed the intestinal mucosal villus degeneration, necrosis, shedding, and inflammatory cell infiltration in the model group, which meant the intestinal mucosal damage models were successfully established. And different concentrations of SPJ protected intestinal mucosa, meanwhile the expressions of GRP78 and TNF- α were significantly reduced in the intestinal epithelial cells as indicated by immunofluorescence staining. Conclusion There is a certain preventive effect of total SPJ on NSAID-induced intestinal injuries via the endoplasmic reticulum stress pathway.

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