# The Water Extract of Sweet Tea Alleviates LPS-Induced Acute Lung Injury Through Anti-Inflammatory and Antioxidant Effects

**Authors:** Haorui Zheng, Taoyu Wang, Hairui Xue, Zihan Zhang, Hengyang Zhang, Yang Cao, Lin Tang

PMC · DOI: 10.3390/nu17213425 · 2025-10-31

## TL;DR

Sweet tea extract reduces lung injury in mice by fighting inflammation and oxidative stress, suggesting potential health benefits.

## Contribution

Identifies sweet tea extract as a novel therapeutic for acute lung injury through anti-inflammatory and antioxidant mechanisms.

## Key findings

- Sweet tea extract reduced lung injury severity and oxidative stress in LPS-induced mouse models.
- WEL inhibited NLRP3, Caspase-1, and GSDMD-NT expression, mitigating cell pyroptosis.
- Phlorizin and trilobatin are potential key active ingredients in sweet tea extract.

## Abstract

Background/Objectives: Lithocarpus litseifolius (Hance) Chun, also known as sweet tea, is a traditional Chinese tea-making plant. Acute lung injury (ALI), a life-threatening syndrome with symptoms like hypoxemia and dyspnea, can be triggered by infection or trauma, with high morbidity and mortality. Whether the water extract of Lithocarpus litseifolius (WEL) has therapeutic effects on ALI remains unclear. This study aimed to analyze WEL’s components, establish in vitro cellular inflammation and mouse ALI models, and investigate WEL’s protective effects against LPS-induced ALI. Methods: LC-MS analysis identified 42 compounds in WEL and quantified three key ones. In an LPS-induced mouse ALI model, WEL significantly reduced lung injury severity, lung wet-to-dry ratio, pulmonary edema, and levels of NO, ROS, IL-1β, TNF-α, and MPO in lung tissues and bronchial alveolar lavage fluid. Immunohistochemical analysis showed WEL pretreatment inhibited the upregulation of NLRP3, Caspase-1, and GSDMD-NT expression, mitigated tissue oxidative stress and cell pyroptosis, and alleviated ALI severity in mice. Cellular experiments confirmed WEL’s protective effects via anti-inflammatory, antioxidant actions, and inhibiting cell pyroptosis, with phlorizin and trilobatin as potential key active ingredients. Conclusions: This research demonstrates sweet tea’s significant protective effects against ALI and its potential to alleviate inflammation by inhibiting pyroptosis, providing a theoretical basis for developing new health-promoting functions of sweet tea.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], Caspase1 (caspase-1) [NCBI Gene 692604]
- **Chemicals:** phlorizin (PubChem CID 6072), trilobatin (PubChem CID 6451798), NO (PubChem CID 24822), MPO (PubChem CID 3270828)
- **Diseases:** acute lung injury (MONDO:0006502), ALI (MONDO:0006502)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Nlrp3 (NLR family, pyrin domain containing 3) [NCBI Gene 216799] {aka AGTAVPRL, AII/AVP, Cias1, FCAS, FCU, MWS}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Casp1 (caspase 1) [NCBI Gene 12362] {aka ICE, Il1bc}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Mpo (myeloperoxidase) [NCBI Gene 17523] {aka mKIAA4033}
- **Diseases:** dyspnea (MESH:D004417), infection (MESH:D007239), ALI (MESH:D055371), trauma (MESH:D014947), lung injury (MESH:D055370), Inflammatory (MESH:D007249), hypoxemia (MESH:D000860), pulmonary edema (MESH:D011654)
- **Chemicals:** Lithocarpus litseifolius (-), phlorizin (MESH:D010695), Water (MESH:D014867), NO (MESH:D009614), trilobatin (MESH:C000598619), LPS (MESH:D008070)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Lithocarpus litseifolius (species) [taxon 425828]

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12609318/full.md

---
Source: https://tomesphere.com/paper/PMC12609318