# Mechanism of Green Tea Peptides in Lowering Blood Pressure and Alleviating Renal Injury Induced by Hypertension Through the Ang II/TGF-β1/SMAD Signaling Pathway

**Authors:** Lulu Li, Shili Sun, Xingfei Lai, Qiuhua Li, Ruohong Chen, Zhenbiao Zhang, Mengjiao Hao, Suwan Zhang, Lingli Sun, Dongli Li

PMC · DOI: 10.3390/nu17081300 · Nutrients · 2025-04-08

## TL;DR

Green tea peptides lower blood pressure and protect kidneys in hypertensive rats by reducing fibrosis and inflammation through specific signaling pathways.

## Contribution

This study identifies green tea peptides as effective agents for hypertension and kidney injury via inhibition of Ang II/TGF-β1/SMAD and MyD88/NF-κB p65/iNOS pathways.

## Key findings

- Green tea peptides reduced systolic and diastolic blood pressure in SHRs by 20–28%.
- Peptides inhibited fibrosis markers like TGF-β1 and alpha-SMA by up to 63% and 86%.
- Renal inflammation was reduced through downregulation of MyD88, iNOS, and NF-κB p65.

## Abstract

Background/Objectives: The kidney plays a crucial role in regulating normal blood pressure and is one of the major organs affected by hypertension. The present study aimed to investigate the hypotensive and renoprotective effects of four specific green tea peptides extracted from green tea dregs on spontaneously hypertensive rats (SHRs) and to investigate the underlying mechanisms. Methods: Four specific green tea peptides (40 mg/kg) were gavaged to SHRs for 4 weeks, and blood pressure, renal function, renal pathological changes, renal tissue fibrosis indexes, and inflammation indexes were examined in SHRs to analyze the role of the four green tea peptides in alleviating hypertension and its renal injury. Results: The results showed that the four TPs significantly reduced systolic and diastolic blood pressure (20–24% and 18–28%) in SHR compared to the model group. Meanwhile, gene levels and protein expression of renal fibrosis-related targets such as phospho-Smad2/3 (p-Smad2/3) (26–47%), Sma- and Mad-related proteins 2/3 (Smad2/3) (19–38%), transforming growth factor-β1 (TGF-β1) (36–63%), and alpha-smooth muscle actin (alpha-SMA) (58–86%) were also significantly reduced. In addition, the reduced expression levels of medullary differentiation factor 88 (MyD88) (14–36%), inducible nitric oxide synthase (iNOS) (58–73%), and nuclear factor-κB p65 (NF-kB p65) (35–78%) in kidneys also confirmed that TPs attenuated renal inflammation in SHR. Therefore, green tea peptides could attenuate the fibrosis and inflammatory responses occurring in hypertensive kidneys by inhibiting the Ang II/TGF-β1/SMAD signaling pathway and MyD88/NF-κB p65/iNOS signaling pathway. Conclusions: The results showed that green tea peptides may be effective candidates for lowering blood pressure and attenuating kidney injury.

## Linked entities

- **Genes:** Smad2/3 (Smad2/3 transcription factor) [NCBI Gene 100313734], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040], Acta2 (actin alpha 2, smooth muscle, aorta) [NCBI Gene 11475], MYD88 (MYD88 innate immune signal transduction adaptor) [NCBI Gene 4615], NOS2 (nitric oxide synthase 2) [NCBI Gene 4843]

## Full-text entities

- **Genes:** Agt (angiotensinogen) [NCBI Gene 24179] {aka ANRT, Ang, AngII, PAT}, Nos2 (nitric oxide synthase 2) [NCBI Gene 24599] {aka Nos2a, iNos}, Myd88 (MYD88, innate immune signal transduction adaptor) [NCBI Gene 301059], Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 59086] {aka Tgfb}, Actg2 (actin gamma 2, smooth muscle) [NCBI Gene 25365] {aka ACTGE, SMGA}
- **Diseases:** hypotensive (MESH:D007022), hypertensive kidneys (MESH:D007680), Renal Injury (MESH:D007674), fibrosis (MESH:D005355), Blood (MESH:D006402), Hypertension (MESH:D006973), renal pathological (MESH:D002114), inflammation (MESH:D007249)
- **Chemicals:** Green Tea Peptides (-), TPs (MESH:C089984)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12030635/full.md

## References

73 references — full list in the complete paper: https://tomesphere.com/paper/PMC12030635/full.md

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Source: https://tomesphere.com/paper/PMC12030635