Article Synopsis

  • Radiation therapy (RT) for early colorectal cancer can harm normal tissues through reactive oxygen species, prompting the need for protective measures.
  • Puffed ginseng extract (PGE) shows significant protective effects against RT-induced colorectal injury in mice, outperforming white ginseng extract (WGE) due to higher concentrations of beneficial compounds.
  • PGE mitigates cell death from radiation by regulating apoptotic signaling pathways and reducing oxidative stress, establishing it as a promising radioprotective agent.

Video Abstracts
Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Although radiation therapy (RT) is a feasible treatment approach for early colorectal cancer, RT is considerably toxic to normal tissues due to the increased reactive oxygen species production, which can induce tissue damage. Ginseng, a natural antioxidant agent, exhibits the protective effects against ionizing radiation (IR)-induced damage in and models. The explosive puffing of ginseng has been investigated as a process to improve the efficacy of ginseng due to the resulting physicochemical changes in its functional components. In this study, we provided the evidence for promotion in the beneficial role of puffed ginseng extract (PGE) and associated mechanisms of action, in comparison with white ginseng extract (WGE), against IR-induced colorectal injury, using study on a mouse model. To study the role of PGE in preventing IR-induced damage, we examined colorectal injury and apoptotic changes in mice exposed to Cs at 8 Gy. High-performance liquid chromatography analysis showed that PGE had an increased total ginsenoside concentration with new generation of Rg3, Rg5, and Rk1, compared with the concentrations in WGE. Administering PGE, but not WGE, significantly ameliorated IR-induced colorectal cell death through negative regulation of apoptotic signaling pathways. These antiapoptotic effects of PGE were linked to the capacity to suppress the p53-mediated DNA damage response and NF-B-mediated apoptotic signaling. Moreover, IR-induced oxidative stress in the colorectal epithelium was markedly reduced by PGE administration. Collectively, this study establishes a mechanism of action by which PGE counteracts IR-induced colorectal injury as a novel radioprotective agent.

Download full-text PDF

Source
http://dx.doi.org/10.1089/jmf.2018.4293DOI Listing

Publication Analysis

Top Keywords

ir-induced colorectal
12
colorectal injury
12
puffed ginseng
8
ir-induced damage
8
ginseng extract
8
apoptotic signaling
8
pge
7
ginseng
6
colorectal
6
ir-induced
6

Similar Publications

Purpose: Radiation therapy has revolutionized the treatment of primary or liver metastases in colorectal cancer (CRC). In colorectal cancer, conventional fractionation (1.8 ~ 2.

View Article and Find Full Text PDF

ATRX loss inhibits DDR to strengthen radio-sensitization in p53-deficent HCT116 cells.

Sci Rep

January 2025

NHC Key Laboratory of Radiobiology (Jilin University), School of Public Health, Jilin University, Changchun, 130021, Jilin, People's Republic of China.

Identifying novel targets for molecular radiosensitization is critical for improving the efficacy of colorectal cancer (CRC) radiotherapy. Alpha-thalassemia/mental retardation X-linked (ATRX), a member of the SWI/SNF-like chromatin remodeling protein family, functions in the maintenance of genomic integrity and the regulation of apoptosis and senescence. However, whether ATRX is directly involved in the radiosensitivity of CRC remains unclear.

View Article and Find Full Text PDF

Polymorphism in the Hsa-miR-4274 seed region influences the expression of PEX5 and enhances radiotherapy resistance in colorectal cancer.

Front Med

October 2024

State Key Laboratory of Molecular Oncology, Department of Etiology and Carcinogenesis, Beijing Key Laboratory for Carcinogenesis and Cancer Prevention, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical Co

Identifying biomarkers for predicting radiotherapy efficacy is crucial for optimizing personalized treatments. We previously reported that rs1553867776 in the miR-4274 seed region can predict survival in patients with rectal cancer receiving postoperative chemoradiation therapy. Hence, to investigate the molecular mechanism of the genetic variation and its impact on the radiosensitivity of colorectal cancer (CRC), in this study, bioinformatics analysis is combined with functional experiments to confirm peroxisomal biogenesis factor 5 (PEX5) as a direct target of miR-4274.

View Article and Find Full Text PDF

Background: Tucatinib (TUC), a HER2-directed tyrosine kinase inhibitor, is the first targeted drug demonstrating intracranial efficacy and significantly prolonged survival in metastatic HER2-positive breast cancer (BC) patients with brain metastases. Current treatments for brain metastases often include radiotherapy, but little is known about the effects of combination treatment with TUC. Therefore, we examined the combined effects of irradiation and TUC in human HER2-overexpressing BC, non-small cell lung cancer (NSCLC), and colorectal cancer (CRC) cell lines.

View Article and Find Full Text PDF

Inhibition of DNA-dependent protein kinase (DNA-PK) in the non-homologous end-joining repair pathway reportedly increases the radiation sensitivity of cancer cells. We have recently reported that BR101801, a novel triple inhibitor of PI3K-gamma (γ), delta (δ), and DNA-PK, functions as an efficient sensitizer of radiation-induced DNA damage in various human solid cancer cells and a xenograft mouse model. Given that the p53 tumor suppressor gene plays an important role in radiotherapeutic efficacy, in the current study, we focused on the impact of the p53 status on BR101801-induced radiosensitization using isogenic HCT116 p53 and HCT116 p53 human colorectal cancer cell lines.

View Article and Find Full Text PDF