Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education and Yunnan Province, School of Chemical Science and Technology, Yunnan University, Kunming, Yunnan, 650091, China.
State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming, Yunnan, 650201, China.
Sci Rep. 2020 Mar 16;10(1):4783. doi: 10.1038/s41598-020-61794-6.
Epigallocatechin-3-gallate (EGCG), a main active catechin in green tea, was reported to attenuate renal injury and hypertension. However, its effects on salt-induced hypertension and renal injury remain unclear. In the present study, we explored its effects on hypertension and renal damage in Dahl rats with salt-sensitive hypertension. We found that EGCG could lower blood pressure after 6 weeks of oral administration, reduce 24 h urine protein levels and decrease creatinine clearance, and attenuate renal fibrosis, indicating that it could attenuate hypertension by protecting against renal damage. Furthermore, we studied the renal protective mechanisms of EGCG, revealing that it could lower malondialdehyde levels, reduce the numbers of infiltrated macrophages and T cells, and induce the apoptosis of NRK-49F cells. Considering that the 67 kD laminin receptor (67LR) binds to EGCG, its role in EGCG-induced fibroblast apoptosis was also investigated. The results showed that an anti-67LR antibody partially abrogated the apoptosis-inducing effects of EGCG on NRK-49F cells. In summary, EGCG may attenuate renal damage and salt-sensitive hypertension via exerting anti-oxidant, anti-inflammatory, and apoptosis-inducing effects on fibroblasts; the last effect is partially mediated by 67LR, suggesting that EGCG represents a potential strategy for treating salt-sensitive hypertension.
表没食子儿茶素没食子酸酯（EGCG）是绿茶中主要的活性儿茶素，据报道可减轻肾损伤和高血压。然而，其对盐诱导的高血压和肾损伤的影响尚不清楚。在本研究中，我们探讨了其对盐敏感性高血压 Dahl 大鼠高血压和肾损伤的影响。我们发现 EGCG 经口服给药 6 周后可降低血压，降低 24 小时尿蛋白水平和肌酐清除率，并减轻肾纤维化，表明其可通过保护肾脏来减轻高血压。此外，我们研究了 EGCG 的肾保护机制，发现它可以降低丙二醛水平，减少浸润的巨噬细胞和 T 细胞数量，并诱导 NRK-49F 细胞凋亡。鉴于 67kD 层粘连蛋白受体（67LR）与 EGCG 结合，还研究了其在 EGCG 诱导成纤维细胞凋亡中的作用。结果表明，抗 67LR 抗体部分阻断了 EGCG 对 NRK-49F 细胞的凋亡诱导作用。总之，EGCG 可能通过对成纤维细胞发挥抗氧化、抗炎和诱导凋亡作用来减轻肾损伤和盐敏感性高血压；最后一种作用部分通过 67LR 介导，提示 EGCG 可能是治疗盐敏感性高血压的一种潜在策略。
