Journal of ethnopharmacology · 2025
Huang-qin decoction alleviates deoxycholic acid-induced colorectal cancer in mice by regulating gut microbiota.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Yujing, Zhang Qiang, Lu Lu, Qian Yufan, Wu Yuanmin, Hu Dan, Xu Yangxian, Xu Hanchen, Ji Guang
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Huangqin Decoction (HQD), a traditional Chinese medicine (TCM) formula documented in Shang Han Lun, has demonstrated safety and efficacy in the treatment of ulcerative colitis (UC). Recent studies also suggest that HQD exerts therapeutic effects on colorectal cancer (CRC). However, the underlying mechanisms remain unclear.
AIMS OF THE STUDY: This study aimed to investigate the therapeutic effects of HQD on CRC and explore its potential mechanisms of action.
METHODS: The active ingredients and potential targets of HQD were identified through network pharmacology-based analyses. The CRC-related targets were compared with those of HQD. Shared targets were subjected to Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and a protein-protein interaction (PPI) network was constructed. Additionally, APCmin/+ mice were treated with 0.2 % deoxycholic acid (DCA) and gavaged with low or high doses of HQD. Tumor morphology was assessed using hematoxylin and eosin (HE) staining. Immunohistochemical staining was performed to evaluate the expression of Ki-67, Caspase-3, and MUC2 in the intestine. Periodic acid-Schiff (PAS) and PAS-alcian blue (PAS-AB) staining were utilized to detect mucin distribution and the number of goblet cells in the intestines of the mice. The mRNA expression levels of interleukin 6 (IL-6), mitogen-activated protein kinase 8 (MAPK8), vascular endothelial growth factor A (VEGFA), epidermal growth factor receptor (EGFR), albumin (ALB), and Caspase 3 (CASP3) were quantified using quantitative reverse-transcription PCR (qRT-PCR). Immunofluorescence was employed to assess the degree of apoptosis. Additionally, 16S ribosomal RNA gene sequencing, sequence curation and annotation, and metagenomic sequencing were performed to analyze changes in the composition of the mouse intestinal microbiota and related functions and signaling pathways.
RESULTS: The active ingredients of HQD were identified. GO and KEGG pathway enrichment analyses indicated that the shared targets were primarily involved in tumor suppression. HQD effectively treated DCA-induced CRC in mice. Furthermore, positive PAS and PAS-AB staining was significantly increased in the intestines of mice treated with HQD. HQD enhanced the abundance of Lachnospiraceae, Firmicutes, Fusobacteria, and Clostridium, while reducing the abundance of Eggerthellales. Additionally, HQD modulated secondary bile acid metabolism, carbohydrate synthesis, and other energy metabolism pathways, which may underlie its therapeutic effects.
CONCLUSION: HQD effectively treated CRC in mice, and its mechanisms of action may be related to the regulation of the gut microbiota.
AIMS OF THE STUDY: This study aimed to investigate the therapeutic effects of HQD on CRC and explore its potential mechanisms of action.
METHODS: The active ingredients and potential targets of HQD were identified through network pharmacology-based analyses. The CRC-related targets were compared with those of HQD. Shared targets were subjected to Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and a protein-protein interaction (PPI) network was constructed. Additionally, APCmin/+ mice were treated with 0.2 % deoxycholic acid (DCA) and gavaged with low or high doses of HQD. Tumor morphology was assessed using hematoxylin and eosin (HE) staining. Immunohistochemical staining was performed to evaluate the expression of Ki-67, Caspase-3, and MUC2 in the intestine. Periodic acid-Schiff (PAS) and PAS-alcian blue (PAS-AB) staining were utilized to detect mucin distribution and the number of goblet cells in the intestines of the mice. The mRNA expression levels of interleukin 6 (IL-6), mitogen-activated protein kinase 8 (MAPK8), vascular endothelial growth factor A (VEGFA), epidermal growth factor receptor (EGFR), albumin (ALB), and Caspase 3 (CASP3) were quantified using quantitative reverse-transcription PCR (qRT-PCR). Immunofluorescence was employed to assess the degree of apoptosis. Additionally, 16S ribosomal RNA gene sequencing, sequence curation and annotation, and metagenomic sequencing were performed to analyze changes in the composition of the mouse intestinal microbiota and related functions and signaling pathways.
RESULTS: The active ingredients of HQD were identified. GO and KEGG pathway enrichment analyses indicated that the shared targets were primarily involved in tumor suppression. HQD effectively treated DCA-induced CRC in mice. Furthermore, positive PAS and PAS-AB staining was significantly increased in the intestines of mice treated with HQD. HQD enhanced the abundance of Lachnospiraceae, Firmicutes, Fusobacteria, and Clostridium, while reducing the abundance of Eggerthellales. Additionally, HQD modulated secondary bile acid metabolism, carbohydrate synthesis, and other energy metabolism pathways, which may underlie its therapeutic effects.
CONCLUSION: HQD effectively treated CRC in mice, and its mechanisms of action may be related to the regulation of the gut microbiota.