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Archive > Volume 33 Issue 2 > 2026,33(2):190-198. DOI:10.3872/j.issn.1007-385X.2026.02.011 Prev Next
Basic Research
Effect of epigallocatechin gallate on gut microbiota during hepatocarcinogenesis in rats
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Abstract:
[Abstract] Objective: To investigate the effect of the green tea polyphenol epigallocatechin gallate (EGCG) on the structural changes of gut microbiota during hepatocarcinogenesis in rats. Method: A Sprague-Dawley (SD) rat model of hepatocellular carcinoma (HCC) induced by diethylnitrosamine (DEN) was established. Twenty-six SD rats were randomly divided into three groups: normal control group, HCC model group and EGCG intervention group. Starting from day 1, the EGCG group received daily intragastric administration of EGCG (40 mg/kg), while the normal control and HCC model groups received an equal volume of saline, once daily for 20 weeks. At the end of the experiment, fecal samples were collected for DNA extraction and high-throughput sequencing of the 16S rRNA gene V3-V4 region. Rats were then euthanized, livers were collected to observe tumor formation, and the incidence of HCC was calculated equencing data were processed to generate an operational taxonomic unit (OTU) table. Alpha diversity (Observed species, Chao1, Shannon, Simpson) and beta diversity were analyzed, followed by taxonomic annotation to identify compositional differences in gut microbiota among groups. Results: The liver tumor formation rate was significantly lower in the EGCG intervention group (n = 8) compared to the HCC model group (n = 10) (50% vs 100%, P = 0.023), with no tumors observed in the normal control group (n = 8). In terms of gut microbiota, the number of operational taxonomic units (OTU) in the HCC model group was significantly lower than that in the normal control group (P < 0.001), while the OTU number in the EGCG intervention group was significantly higher than that in the HCC model group (P = 0.021). Alpha diversity analysis revealed that the Shannon index was lower in the HCC model group compared to the normal control group (P < 0.05). Furthermore, compared to the HCC model group, the EGCG intervention group showed significant increases in the Observed species, Chao1, Shannon, and Simpson indices (P < 0.05). Beta diversity analysis, based on principal coordinate analysis (PCoA) and PERMANOVA (R2 = 0.3918, P = 0.001), indicated a significant separation of the gut microbiota structure among the three groups. The microbial community structure of the EGCG intervention group was positioned between the HCC model and normal control groups, clustering closer to the normal controls. The HCC model group exhibited an enrichment of potential pathobionts (e.g., Streptococcus) and a significant reduction in the abundance of butyrate-producing bacteria (e.g., Butyricicoccus, Ruminococcus) (P < 0.05) compared to the normal controls. In contrast, EGCG intervention resulted in a more stable gut microbiota structure during hepatocarcinogenesis, characterized by a significantly increased Firmicutes/Bacteroidota ratio (P < 0.05), and an enrichment of beneficial bacteria (e.g., Bifidobacterium, Lactobacillus) and butyrate-producing bacteria (e. g., Butyricicoccus). Conclusion: EGCG intervention reduces the incidence of DEN-induced HCC in rats and helps stabilize the gut microbiota structure. This effect may be associated with increased microbial diversity, promotion of beneficial and butyrate-producing bacteria, and restoration of microbial balance.
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