Journal of Physiology & Pathology in Korean Medicine (동의생리병리학회지)

The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine (대한동의생리학회·한의병리학회)
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Effect of Korean Red Ginseng Crude Saponin on Di(2-ethylexylphthalate)-induced Respiratory Toxicity

고려홍삼의 조사포닌이 Di(2-ethylexyl phthalate에 의해 유발된 호흡기독성에 미치는 영향

  • Seung Hwa Baek (Department of Biomedical Laboratory Science, Daejeon University) ;
  • Ji Hye Oh (Department of Biomedical Laboratory Science, Daejeon University) ;
  • Hee Won Seo (Department of Biomedical Laboratory Science, Daejeon University) ;
  • Seock Yeon Hwang (Department of Biomedical Laboratory Science, Daejeon University)
  • 백승화 (대전대학교 임상병리학과) ;
  • 오지혜 (대전대학교 임상병리학과) ;
  • 서희원 (대전대학교 임상병리학과) ;
  • 황석연 (대전대학교 임상병리학과)
  • Received : 2024.04.15
  • Accepted : 2024.08.20
  • Published : 2024.08.25
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Abstract

Phthalates are used as plasticizers in plastics and other products, including household goods, and enter the human body mainly through oral, inhalation, and skin. Saponins in Korean red ginseng are known to have immune enhancement, central nervous system protection, anticancer, and anti-inflammatory properties. Therefore, the present study aimed to investigate the protective effects of Crude-saponin administration against DEHP-induced respiratory toxicity. A DEHP-induced respiratory toxicity model was performed using prepubertal 4-week-old SD rats, and the inflammatory response of blood and tissues obtained through autopsy was analyzed to determine the toxicity of DEHP and the protective effect of Crude-saponins against it. The results showed that MUC5AC and CCR3 were consistently increased in the DEHP-treated model, as well as the expression of key respiratory mucins. The inflammatory cytokines IL-13 and IL-5 increased, and TARC, which is responsible for Th2 migration, also tended to increase. However, the above phenomena gradually decreased in a concentration-dependent manner in the Crude-saponin-treated group. These results confirm that Crude-saponins are involved in gene protein expression inhibition and stress-induced mechanisms in respiratory injury. The expression of key respiratory mucins was consistently increased in the DEHP treatment model. As DEHP-induced impairment of NF-κB/MAPK signaling has been reported, further in vitro studies are needed to investigate the mechanisms involved in upstream signaling.

Keywords

References

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