Journal of ginseng research · 2025
Korean red ginseng extract inhibits microplastic translocation via the gut-liver axis by ameliorating alcohol-induced intestinal disruption.
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Baek Su-Min, Lee Young-Jin, Yim Jae-Hyuk, Kim Tae-Un, Kim Woo Jun, Lee Seoung-Woo, Kim Hee-Yeon, Kang Kyung-Ku, Lee Kyeong-Min, Choi Seong-Kyoon, Kim Sung Dae, Rhee Man-Hee, Park Jin-Kyu
Аннотация
BACKGROUND: Impaired intestinal mucosal barrier in alcoholic liver disease leads to the entry of toxic substances into the liver parenchyma. Ingestion of microplastics (MPs; plastic particles sized <5 mm) can induce inflammation, metabolic disorders, oxidative stress, and cancer. Red ginseng extract (RGE) is a widely used herbal medicine globally. The effects of RGE on the accumulation of MPs and the underlying mechanisms remain unclear.
METHODS: Nine-week-old male wild-type C57BL/6 mice were fed a control liquid diet or ethanol diet with or without MP and RGE. MPs (fluorescent-tagged 2.16-μm polystyrene MP; dose: 0.1 mg/kg body weight) and RGE (dose: 250 or 500 mg/kg body weight) were orally administered five times a week.
RESULTS: RGE treatment markedly reduced MP accumulation in the liver and intestines. In the intestines, RGE protected tight junctions, as shown by ZO-1 and F-actin expression, and prevented MP translocation into the lamina propria. It also inhibited ethanol- and MP-induced villi fusion, epithelial detachment, and vacuolization. In the liver, RGE attenuated ethanol-mediated steatosis, lobular inflammation, and ballooning degeneration. In vitro, RGE restored tight junction integrity in Caco-2 cells by upregulating ZO-1 while reducing MP accumulation. However, its effect on goblet cell differentiation (MUC-2) in HT-29 cells was minimal, suggesting that in vivo goblet cell regeneration occurred secondarily to tight junction protection.
CONCLUSION: Disruption of the gut-liver axis leads to increased translocation of MPs into the lamina propria and their secondary accumulation in the intestines and liver. RGE inhibits the accumulation of MPs by protecting the intestinal epithelial mucosal barrier.
METHODS: Nine-week-old male wild-type C57BL/6 mice were fed a control liquid diet or ethanol diet with or without MP and RGE. MPs (fluorescent-tagged 2.16-μm polystyrene MP; dose: 0.1 mg/kg body weight) and RGE (dose: 250 or 500 mg/kg body weight) were orally administered five times a week.
RESULTS: RGE treatment markedly reduced MP accumulation in the liver and intestines. In the intestines, RGE protected tight junctions, as shown by ZO-1 and F-actin expression, and prevented MP translocation into the lamina propria. It also inhibited ethanol- and MP-induced villi fusion, epithelial detachment, and vacuolization. In the liver, RGE attenuated ethanol-mediated steatosis, lobular inflammation, and ballooning degeneration. In vitro, RGE restored tight junction integrity in Caco-2 cells by upregulating ZO-1 while reducing MP accumulation. However, its effect on goblet cell differentiation (MUC-2) in HT-29 cells was minimal, suggesting that in vivo goblet cell regeneration occurred secondarily to tight junction protection.
CONCLUSION: Disruption of the gut-liver axis leads to increased translocation of MPs into the lamina propria and their secondary accumulation in the intestines and liver. RGE inhibits the accumulation of MPs by protecting the intestinal epithelial mucosal barrier.