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Phytomedicine, Available online 17 May 2026 | https://doi.org/10.1016/j.phymed.2026.158318 Ginsenoside Rd attenuates fine particulate matter-induced pulmonary inflammation by directly inhibiting the transforming growth factor-beta-activated kinase 1-mediated toll-like receptor 2 signaling

Yu Na Song^a,b,1, Su Hyeon Yun ^a,c,1, Seung-Hyung Kim^d,1, Eun Sol Oh ^a, Hong-Hee Kim ^a,c, Hyung Won Ryu ^a, Soo Jin Oh ^e, Ji-Yoon Lee^e, Sooil Kim^c, Seunghoon Yang ^f,g, Jinhyuk Lee ^f,g, Hyunju Ro ^b, Sung-Tae Hong ^c, Su Ui Lee ^a

^aNatural Product Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju 28116, Republic of Korea
^bDepartment of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Republic of Korea
^cDepartments of Anatomy & Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea
^dDJU Industry-University Cooperation Foundation, Daejeon University, Daejeon 34520, Republic of Korea
^eAsan Institute for Life Sciences, Asan Medical Center, Department of Pharmacology, College of Medicine, University of Ulsan, Seoul, 05505, Republic of Korea
^fBio Design Editing Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 34141, Republic of Korea
^gDepartment of Bioinformatics, KRIBB School of Bioscience, University of Science and Technology (UST), Daejeon, 34113, Republic of Korea

¹These authors contributed equally to this work.
Corresponding author: Hyunju Ro, Sung-Tae Hong, Su Ui Lee

Abstract

Background
Particulate matter (PM) exposure is a major risk factor for the progression and exacerbation of inflammatory lung diseases. Ginsenoside Rd, a bioactive compound derived from Panax ginseng, has been reported to improve lung function; however, its effects on PM2.5 (PM less than 2.5 μm in diameter)-induced pulmonary inflammation and the underlying molecular mechanisms remain unclear.

Purpose
This study investigated whether ginsenoside Rd mitigates PM2.5-induced lung inflammation and explored its molecular targets in vitro and in vivo.
Methods
Mouse alveolar macrophages were stimulated with PM2.5, and mice were exposed to a PM10 and diesel exhaust particles mixture (PM/DEP) to evaluate the anti-inflammatory effects of ginsenoside Rd. Levels of TNF-α, IL-6, neutrophil elastase, immune cell infiltration, Toll-like receptor 2 (TLR2) expression, and transforming growth factor β-activated kinase 1 (TAK1) signaling were assessed. Histological staining was performed to examine lung tissue morphology. The direct interaction between Rd and TAK1 was also analyzed.

Results
In vitro, ginsenoside Rd reduced TNF-α, IL-6, and TLR2 expression by inhibiting TAK1-dependent activation of the IκB kinase (IKK)/nuclear factor-κB (NF-κB) and extracellular signal-regulated kinase (ERK)/cAMP response element-binding protein (CREB) pathways. In vivo, Rd attenuated PM/DEP-induced lung tissue damage and neutrophil infiltration, thereby suppressing pulmonary inflammation via blockade of the TAK1/NF-κB pathway. Binding assays confirmed a direct interaction between Rd and TAK1, supporting its role as the key molecular target.

Conclusion
Ginsenoside Rd exerts protective effects against PM2.5-induced pulmonary inflammation by directly inhibiting TAK1-mediated TLR2 signaling. These findings suggest its potential as a therapeutic candidate for inflammatory lung diseases aggravated by air pollution.

논문소개전체 설명

미세먼지(PM2.5)는 현대 사회에서 누구나 쉽게 노출될 수 있는 대표적인 환경 유해인자로, 장기간 노출 시 폐 염증과 만성 호흡기 질환을 유발하는 것으로 알려져 있다. 특히 미세먼지는 폐 조직 내 선천면역 반응을 과도하게 활성화시키며 다양한 염증성 signaling pathway를 자극한다. 이러한 배경에서 본 연구에서는 인삼 유래 사포닌 성분인 ginsenoside Rd가 미세먼지에 의해 유도되는 폐 염증 반응을 조절할 수 있는지에 주목하였다.

연구 결과, ginsenoside Rd는 미세먼지 노출로 증가한 염증세포 침윤과 염증성 사이토카인 발현을 효과적으로 감소시켰으며, 폐 조직 손상 역시 완화시키는 것을 확인하였다. 특히 본 연구에서는 Rd가 단순한 항산화 또는 비특이적 항염증 효과를 나타내는 것이 아니라, TLR2 signaling의 핵심 조절 인자인 TAK1(transforming growth factor-beta-activated kinase 1)에 직접 작용하여 downstream inflammatory signaling을 억제한다는 점을 규명하였다.

흥미로운 점은, 다양한 TLR signaling 중에서도 TLR2-mediated inflammatory pathway를 선택적으로 조절하였다는 점이다. 미세먼지 유래 염증 반응은 여러 선천면역 경로가 복합적으로 관여하는 것으로 알려져 있는데, 본 연구는 그중에서도 TAK1과 TLR2를 중심으로 한 보다 구체적인 기전을 제시하였다는 점에서 의미가 있다. 이는 천연물 유래 소재가 단순한 broad anti-inflammatory 효과를 넘어 특정 염증 signaling pathway를 직접 조절할 수 있음을 보여주며, 향후 미세먼지로 인한 만성 호흡기 질환의 예방 및 치료 전략 개발에 새로운 가능성을 제시한다.

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