Bibliographic Details
| Title: |
Inhibitory Effect and Mechanism of Lentinan on Colitis-Associated Colorectal Cancer Induced by AOM/DSS Through IL-6/STAT3 Pathway |
| Authors: |
Junjie LIU, Jia LIANG, Tianshu PANG, Jialong XUE, Dechun LIU |
| Source: |
Zhongliu Fangzhi Yanjiu, Vol 51, Iss 11, Pp 908-912 (2024) |
| Publisher Information: |
Magazine House of Cancer Research on Prevention and Treatment, 2024. |
| Publication Year: |
2024 |
| Collection: |
LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens |
| Subject Terms: |
lentinan, colitis-associated colorectal cancer, il-6, stat3, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282 |
| More Details: |
ObjectiveTo investigate the inhibitory effect and mechanism of lentinan on colitis-associated colorectal cancer (CAC) induced by azomethane (AOM)/dextran sulfate sodium salt (DSS) through the IL-6/ STAT3 pathway. MethodsC57BL/6 mice were randomly divided into a control group, a model group, a low-dose group (0.865 mg/kg lentinan), a medium-dose group (1.73 mg/kg lentinan), and a high-dose group (3.46 mg/kg lentinan). Except the control group, CAC was induced by AOM/DSS in the other groups, and corresponding drugs were injected intraperitoneally during the modeling process. Body mass, disease activity index (DAI) score, colon length, and tumor number were compared among all groups. Hematoxylin–eosin staining was used to observe the pathological morphology of colon. ELISA was utilized to detect the IL-6, IL-1β, and IL-18 contents in serum. Western blot analysis was conducted to detect the expression levels of IL-6, p-STAT3, and c-Myc in colon tissues. ResultsThe tumor number, DAI score, serum IL-6, IL-1β, and IL-18 contents and the expression levels of IL-6, p-STAT3, and c-Myc in the colon tissue of the model group were higher than those of the control group, while the body mass and colon length were lower than those of the control group (P |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
Chinese |
| ISSN: |
1000-8578 |
| Relation: |
https://doaj.org/toc/1000-8578 |
| DOI: |
10.3971/j.issn.1000-8578.2024.24.0340 |
| Access URL: |
https://doaj.org/article/221075548418424da913c1bd98c66a76 |
| Accession Number: |
edsdoj.221075548418424da913c1bd98c66a76 |
| Database: |
Directory of Open Access Journals |
