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Original Research Article | OPEN ACCESS

Chrysophanol exerts protective effect against atherosclerosis via NFκB-mediated signaling in LDLR-/- mice model

Yuping Li, Jun Zhang, Huawei Tian

Department of Cardiology, Xiangyang No. 1 People’s Hospital, Hubei University of Medicine, Xiangyang, Hubei, China, 441000;

For correspondence:-  Huawei Tian   Email: 13523754@qq.com   Tel:+867103420031

Accepted: 27 March 2022        Published: 30 April 2022

Citation: Li Y, Zhang J, Tian H. Chrysophanol exerts protective effect against atherosclerosis via NFκB-mediated signaling in LDLR-/- mice model. Trop J Pharm Res 2022; 21(4):741-747 doi: 10.4314/tjpr.v21i4.9

© 2022 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 study the therapeutic effect of chrysophanol (CHR) on diet-induced atherogenesis in LDLR-/- mice.
Methods: Mice were fed atherogenic diet for 12 weeks after which some lipid profile markers such as total cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c) and triglyceride (TG) were measured. The mRNA expression levels of lipid synthesis genes and lipid overload-related inflammatory indicator molecules were assayed with quantitative real time polymerase chain reaction (qRT-PCR), while the corresponding protein expressions were determined with western blotting assay. The therapeutic effect of CHR on atherogenesis was confirmed using H & E and Oil red O stainings of mice aortic sections.
Results: CHR administration significantly reduced levels of TC, LDL-c, HDL-c and TG (p ≤ 0.05), and restored the mRNA and protein expressions of genes involved in lipid and glucose homeostasis, namely, AdipoR1, PPAR-? and HMco-A (p < 0.05). Moreover, CHR potentially alleviated diet-induced inflammation, as is evident in reduced levels of molecular inflammatory signaling factors NF-κB and TLR-4, and significant down-regulations of the proinflammatory cytokines, TNF-α, IL-6 and IL-1β (p < 0.05). Furthermore, aorta histology revealed that CHR significantly reduced lipid storage in the arteries of mice fed atherogenic diet (p < 0.05).
Conclusion: These results indicate that CHR reduces diet-induced lipid storage in LDLR-/- mice and also controlled inflammation-associated lipid overload. These findings may provide a molecular basis for potential application of chrysophanol in the treatment of atherosclerosis.

Keywords: Chrysophanol, Inflammation, Atherosclerosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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