Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Protective effect of crocin on chronic heart failure and its mechanism of action

Yali Hu¹ , Jie Yang¹, Qianqian Pang¹, Pengpeng Zhang², Keqin Liu¹

¹Department of Pharmacy, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, China; ²Zhangjiakou Drug Rehabilitation Center, Zhangjiakou, Hebei, China.

For correspondence:- Yali Hu Email: chuyijiutu08939@163.com

Accepted: 12 December 2022 Published: 31 January 2023

Citation: Hu Y, Yang J, Pang Q, Zhang P, Liu K. Protective effect of crocin on chronic heart failure and its mechanism of action. Trop J Pharm Res 2023; 22(1):113-120 doi: 10.4314/tjpr.v22i1.16

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To explore the mechanism of action of crocin in rat chronic heart failure (CHF).

Methods: One hundred male Sprague Dawley (SD) rats were used to establish CHF rat model by the abdominal aorta constriction method. They were equally randomized into either the model control group (injected with distilled water), crocin low, medium, and high dose groups (daily administered 0.05, 0.1, and 0.75 g/kg of crocin, respectively), or positive control group (daily administration of benazepril hydrochloride), and normal control (without treatment). Parameters evaluated include heart function, inflammatory index changes, and oxidative stress damage.

Results: The crocin low, medium, and high dose groups and the positive control group had significantly better cardiac function indices versus the model control group (p < 0.05). High-dose crocin resulted in significantly lower levels of inflammatory factors than a low or medium dose (p < 0.05). Rats that received a medium or high dose of crocin showed significantly increased activity of myocardial antioxidant enzymes, and reduced malondialdehyde (MDA) and reactive oxygen species (ROS) content when compared to those given low doses of crocin (p < 0.05). Protein expressions of Bax-activated caspase-3, and NF-kB decreased significantly with increase in crocin dosage. A high dose of crocin produced a significantly lower apoptotic rate of cardiomyocytes, sodium–calcium exchanger (NCX) level and higher content of sarcoplasmic reticulum calcium pump 2a (SERCA2a) compared with low- and medium-doses.

Conclusion: Crocin protects myocardial tissue and enhances ventricular diastolic function of CHF rats through down-regulation of NCX expression and up-regulation of SERCA2a expression. Further studies using clinical CHF models to categorize and analyze crocin-related cellular pathways will be required.

Keywords: Crocin, Chronic heart failure, Protective effect, Mechanism of action