Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway
Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma c...
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| Format: | Article |
| Language: | English |
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PAGEPress Publications
2025-01-01
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| Series: | European Journal of Histochemistry |
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| Online Access: | https://www.ejh.it/index.php/ejh/article/view/4158 |
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| author | Mei Yang Wangbin Xu Chaofu Yue Rong Li Xian Huang Yongjun Yan Qinyong Yan Shisheng Liu Yuan Liu Qiaolin Li |
| author_facet | Mei Yang Wangbin Xu Chaofu Yue Rong Li Xian Huang Yongjun Yan Qinyong Yan Shisheng Liu Yuan Liu Qiaolin Li |
| author_sort | Mei Yang |
| collection | DOAJ |
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Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma cell line Caco-2 and rats were treated with lipopolysaccharide (LPS) to establish in vitro and in vivo models, respectively, of intestinal barrier damage. The expression of inflammatory cytokines (TNF-α, HMGB1, IL-1β and IL-6), antioxidant enzymes (iNOS, SOD and CAT), and oxidative products (MDA and 8-iso-PGF2α) was detected using ELISA kits and related reagent kits. Apoptosis-related proteins (Bcl-2, Bax, Caspase-3 and Caspase-9), tight junction proteins (ZO-1, Occludin, E-cadherin, and Claudin-1) and p38 MAPK pathway-associated protein were detected by Western blotting. In addition, cell viability and apoptosis was determined by a CCK-8 kit and flow cytometry, respectively. Cell permeability was assayed by the transepithelial electrical resistance value and FITC-dextran concentration. The homing effect of ADSCs was detected by fluorescence labeling, and intestinal barrier tissue was observed by HE staining. After ADSC treatment, the level of phosphorylated p38 MAPK protein decreased, the expression of inflammatory factors, oxidative stress and cell apoptosis decreased, the expression of tight junction proteins increased, and cell permeability decreased in Caco-2 cells stimulated with LPS. In rats, ADSCs are directionally recruited to damaged intestinal tissue. ADSCs significantly decreased the levels of D-lactate, diamine oxidase (DAO) and FITC-dextran induced by LPS. ADSCs promoted tight junction proteins and inhibited oxidative stress in intestinal tissue. These effects were reversed after the use of a p38 MAPK activator. ADSCs can be directionally recruited to intestinal tissue, upregulate tight junction proteins, and reduce apoptosis and oxidative stress by inhibiting the p38MAPK signaling pathway. This study provides novel insights into the treatment of intestinal injury.
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| format | Article |
| id | doaj-art-ea222a86fe5347c6b553fdc3e3a15633 |
| institution | Kabale University |
| issn | 1121-760X 2038-8306 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | PAGEPress Publications |
| record_format | Article |
| series | European Journal of Histochemistry |
| spelling | doaj-art-ea222a86fe5347c6b553fdc3e3a156332025-01-22T07:51:10ZengPAGEPress PublicationsEuropean Journal of Histochemistry1121-760X2038-83062025-01-0169110.4081/ejh.2025.4158Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathwayMei Yang0Wangbin Xu1Chaofu Yue2Rong Li3Xian Huang4Yongjun Yan5Qinyong Yan6Shisheng Liu7Yuan Liu8Qiaolin Li9Department of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, First Affiliated Hospital of Kunming Medical University, KunmingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, QujingDepartment of Critical Care Medicine, The Qujing No.1 People's Hospital, Qujing Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma cell line Caco-2 and rats were treated with lipopolysaccharide (LPS) to establish in vitro and in vivo models, respectively, of intestinal barrier damage. The expression of inflammatory cytokines (TNF-α, HMGB1, IL-1β and IL-6), antioxidant enzymes (iNOS, SOD and CAT), and oxidative products (MDA and 8-iso-PGF2α) was detected using ELISA kits and related reagent kits. Apoptosis-related proteins (Bcl-2, Bax, Caspase-3 and Caspase-9), tight junction proteins (ZO-1, Occludin, E-cadherin, and Claudin-1) and p38 MAPK pathway-associated protein were detected by Western blotting. In addition, cell viability and apoptosis was determined by a CCK-8 kit and flow cytometry, respectively. Cell permeability was assayed by the transepithelial electrical resistance value and FITC-dextran concentration. The homing effect of ADSCs was detected by fluorescence labeling, and intestinal barrier tissue was observed by HE staining. After ADSC treatment, the level of phosphorylated p38 MAPK protein decreased, the expression of inflammatory factors, oxidative stress and cell apoptosis decreased, the expression of tight junction proteins increased, and cell permeability decreased in Caco-2 cells stimulated with LPS. In rats, ADSCs are directionally recruited to damaged intestinal tissue. ADSCs significantly decreased the levels of D-lactate, diamine oxidase (DAO) and FITC-dextran induced by LPS. ADSCs promoted tight junction proteins and inhibited oxidative stress in intestinal tissue. These effects were reversed after the use of a p38 MAPK activator. ADSCs can be directionally recruited to intestinal tissue, upregulate tight junction proteins, and reduce apoptosis and oxidative stress by inhibiting the p38MAPK signaling pathway. This study provides novel insights into the treatment of intestinal injury. https://www.ejh.it/index.php/ejh/article/view/4158Intestinal barrier damageADSCsp38 MAPKoxidative stressapoptosis |
| spellingShingle | Mei Yang Wangbin Xu Chaofu Yue Rong Li Xian Huang Yongjun Yan Qinyong Yan Shisheng Liu Yuan Liu Qiaolin Li Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway European Journal of Histochemistry Intestinal barrier damage ADSCs p38 MAPK oxidative stress apoptosis |
| title | Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway |
| title_full | Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway |
| title_fullStr | Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway |
| title_full_unstemmed | Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway |
| title_short | Adipose-derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 MAPK signaling pathway |
| title_sort | adipose derived stem cells promote the recovery of intestinal barrier function by inhibiting the p38 mapk signaling pathway |
| topic | Intestinal barrier damage ADSCs p38 MAPK oxidative stress apoptosis |
| url | https://www.ejh.it/index.php/ejh/article/view/4158 |
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