Efficacy Mechanism of Xianlian Jiedu Prescription Against Colorectal Cancer Recurrence vias Regulating Angiogenesis
10.13422/j.cnki.syfjx.20241625
- VernacularTitle:仙连解毒方通过调控血管生成抗结直肠癌复发的疗效机制
- Author:
Yanru XU
1
;
Lihuiping TAO
1
;
Jingyang QIAN
1
;
Weixing SHEN
1
;
Jiani TAN
1
;
Chengtao YU
1
;
Minmin FAN
1
;
Changliang XU
1
;
Yueyang LAI
1
;
Liu LI
1
;
Dongdong SUN
2
;
Haibo CHENG
1
Author Information
1. The First Clinical College， Nanjing University of Chinese Medicine， Nanjing 210023， China
2. Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine in Prevention and Treatment of Tumor， Nanjing 210023， China
- Publication Type:Journal Article
- Keywords:
Xianlian Jiedu prescription;
colorectal cancer;
postoperative recurrence;
angiogenesis;
efficacy mechanism
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(6):79-87
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore effect of Xianlian Jiedu prescription on the recurrence of colorectal cancer （CRC） and investigate the related mechanisms. MethodsA postoperative recurrence model was established in 25 Balb/c mice by injecting CT26 cells subcutaneously into the armpit， followed by surgical removal of 99% of the subcutaneous tumor. The mice were randomly divided into model group， low-dose Xianlian Jiedu prescription （XLJDP-L） group （6.45 g·kg-1·d-1）， medium-dose Xianlian Jiedu prescription （XLJDP-M） group （12.9 g·kg-1·d-1）， high-dose Xianlian Jiedu prescription （XLJDP-H） group （25.8 g·kg-1·d-1）， and 5-fluorouracil （5-FU） group （1×10-3 g·kg-1·d-1）. The mice were euthanized after 14 days of continuous intervention， and recurrent tumor tissue was harvested. Hematoxylin and eosin （HE） staining was used to observe pathological and morphological changes in the recurrent tumor tissue. Immunohistochemistry （IHC） was employed to assess the expression of proliferating cell nuclear antigen （Ki67）， vascular endothelial growth factor （VEGF）， and platelet-endothelial cell adhesion molecule （CD31） in recurrent tumor tissue. The Western blot was used to detect the protein expression levels of angiopoietin-2 （ANG-2）， VEGF， phosphorylated-protein kinase B （p-Akt）， protein kinase B （Akt）， phosphorylated-phosphatidylinositol 3-kinase （p-PI3K）， and phosphatidylinositol 3-kinase （PI3K） in recurrent tumor tissue. ResultsBefore treatment， there were no statistical differences in tumor volume， tumor weight， and body mass among the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group compared to the model group， indicating model stability. After treatment， compared with those in the model group， the tumor volume and tumor weight in the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group were significantly reduced （P<0.01）， showing dose dependency. Meanwhile， there were no significant differences in body weight among the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group compared to the model group. HE staining showed that compared with that in the model group， tumor tissue in the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group had loosely arranged cells， increased intercellular spaces， small and shriveled nuclei， light staining， fewer mitotic figures and atypical nuclei， and increased necrotic areas. IHC showed that compared with those of the model group， the positive rates of Ki67， VEGF， and CD31 in the recurrent tumor tissue of the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group were significantly reduced （P<0.01） in a dose-dependent manner. Western blot results showed that compared with those of the model group， the protein expression levels of ANG-2 and VEGF in the recurrent tumor tissue of the XLJDP-L， XLJDP-M， and XLJDP-H groups and the 5-FU group were significantly downregulated （P<0.05， P<0.01）， and the p-Akt/Akt and p-PI3K/PI3K ratios were significantly decreased in a dose-dependent manner （P<0.05， P<0.01）. ConclusionXianlian Jiedu prescription significantly inhibits the recurrence of CRC in mice after subcutaneous tumor surgery. The mechanism may involve regulating the PI3K/Akt pathway and downregulating key angiogenic proteins such as ANG-2， VEGF， and CD31.
