Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Potential regulatory effects of CXCR2 and CPEB1 on cardiac cachexia

Yang Li¹, Congyu Zhang², Qian Tong¹, Xiaoxing Feng¹

¹Department of Cardiovascular Medicine, The First Hospital of Jilin University; ²Department of Cardiovascular Medicine, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin, 130021, China.

For correspondence:-

Accepted: 17 March 2021 Published: 30 April 2021

Citation: Li Y, Zhang C, Tong Q, Feng X. Potential regulatory effects of CXCR2 and CPEB1 on cardiac cachexia. Trop J Pharm Res 2021; 20(4):709-714 doi: 10.4314/tjpr.v20i4.7

© 2021 The authors.
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Abstract

Purpose: To investigate the effect of C-X-C motif chemokine receptor 2 (CXCR2) and cytoplasmic polyadenylation element binding protein 1 (CPEB1) which are linked to inflammatory and cellular senescence, on cardiac cachexia.

Methods: Early and advanced stages of cardiac cachexia were established in mice using exogenous injection of single doses of growth differentiation factor 11 (GDF11, 3.0 and 6.0 mg/kg, respectively). The expressions of CXCR2 and CPEB1 were assayed using immonohistochemistry and Western blotting.

Results: Following two weeks of GDF11 injection, cardiac tissue mass was reduced by 23 and 39 % in early and advanced stages cardiac cachexia, respectively, in mice. Histology showed progressive loss of cardiac muscle and cardiomyocyte shrinkage in early stage, with extensive cardiac muscle wasting and disruption of cardiac arche structure in the advanced stage. Immunohistochemistry and Western blotting showed that CXCR2 was 4.6 times overexpressed in the initial stage of cachexia, but was restricted to only 2.4-fold overexpression in advanced stage of cardiac cachexia. The results showed that CXCR2 and its higher expression in early stages of cardiac cachexia prepared the cardiac microenvironment for vast changes during which its expression was limited. There were 2.2-fold and 5.5-fold higher expressions of CPEB1 in early and advanced stages of cardiac cachexia, respectively, indicating its role in cardiac muscle wasting and remodelling in cellular senescence.

Conclusion: CXCR2 overexpression modulates extensive cardiac muscle loss in cardiac cachexia, thus affording a strategy for the management of this pathological condition.

Keywords: Cardiac cachexia, Growth differentiation factor 11 (GDF11), C-X-C motif chemokine receptor 2 (CXCR2), Cytoplasmic polyadenylation element binding prot