2. Academic Validation
  3. Emodin alleviates CRS4-induced mitochondrial damage via activation of the PGC1α signaling

Emodin alleviates CRS4-induced mitochondrial damage via activation of the PGC1α signaling

  • Phytother Res. 2024 Jan 10. doi: 10.1002/ptr.8091.
Xin Dong 1 2 3,  Ruijia Wen 1 2 3,  Yuanyuan Xiong 1 2 3,  Xiaotong Jia 1 2 3,  Xiwen Zhang 1 2 3,  Xin Li 1 2 3,  Liangyou Zhang 1 2 3,  Zhibin Li 1 2 3,  Shu Zhang 1 2 3,  Yanna Yu 1 2 3,  Qiang Li 1 2 3,  Xingbo Wu 1 2 3,  Haitao Tu 1 2 3,  Zixin Chen 1 2 3,  Shaoxiang Xian 1 2 3,  Lingjun Wang 1 2 3,  Chao Wang 1 2 3,  Lianqun Jia 4,  Junyan Wang 1 2 3 5,  Gangyi Chen 1 2 3
Affiliations

Affiliations

  • 1 The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 2 Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 3 Guangzhou Key Laboratory of Chinese Medicine for Prevention and Treatment of Chronic Heart Failure, Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 4 Liaoning University of Traditional Chinese Medicine, Shenyang, China.
  • 5 School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.
PMID: 38198804 DOI: 10.1002/ptr.8091
Abstract

Cardiorenal syndrome type 4 (CRS4), a progressive deterioration of cardiac function secondary to chronic kidney disease (CKD), is a leading cause of death in patients with CKD. In this study, we aimed to investigate the cardioprotective effect of emodin on CRS4. C57BL/6 mice with 5/6 nephrectomy and HL-1 cells stimulated with 5% CKD mouse serum were used for in vivo and in vitro experiments. To assess the cardioprotective potential of emodin, we employed a comprehensive array of methodologies, including echocardiography, tissue staining, immunofluorescence staining, biochemical detection, flow cytometry, real-time quantitative PCR, and western blot analysis. Our results showed that emodin exerted protective effects on the function and structure of the residual kidney. Emodin also reduced pathologic changes in the cardiac morphology and function of these mice. These effects may have been related to emodin-mediated suppression of Reactive Oxygen Species production, reduction of mitochondrial oxidative damage, and increase of oxidative metabolism via restoration of PGC1α expression and that of its target genes. In contrast, inhibition of PGC1α expression significantly reversed emodin-mediated cardioprotection in vivo. In conclusion, emodin protects the heart from 5/6 nephrectomy-induced mitochondrial damage via activation of the PGC1α signaling. The findings obtained in our study can be used to develop effective therapeutic strategies for patients with CRS4.

Keywords

PGC1α; cardiorenal syndrome type 4; emodin; mitochondria.

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