Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Cardioprotective Effects of Arjunolic Acid in LPS-Stimulated H9C2 and C2C12 Myotubes via My88-Dependent TLR4 Signaling Pathway

Md. Mahmudul Hasan
ORCID logo ,
Priya Madhavan
* ,
Nur Adelina Ahmad Noruddin
,
Wai Kwan Lau
,
Qamar Uddin Ahmed
ORCID logo ,
Zainul Amiruddin Zakaria
* ,
Aditya Arya
Version 1 : Received: 27 October 2022 / Approved: 28 October 2022 / Online: 28 October 2022 (07:24:06 CEST)

A peer-reviewed article of this Preprint also exists.

Md Mahmudul Hasan, Priya Madhavan, Nur Adelina Ahmad Noruddin, Wai Kwan Lau, Qamar Uddin Ahmed, Aditya Arya & Zainul Amiruddin Zakaria (2023) Cardioprotective effects of arjunolic acid in LPS-stimulated H9C2 and C2C12 myotubes via the My88-dependent TLR4 signaling pathway, Pharmaceutical Biology, 61:1, 1135-1151, DOI: 10.1080/13880209.2023.2230251 Md Mahmudul Hasan, Priya Madhavan, Nur Adelina Ahmad Noruddin, Wai Kwan Lau, Qamar Uddin Ahmed, Aditya Arya & Zainul Amiruddin Zakaria (2023) Cardioprotective effects of arjunolic acid in LPS-stimulated H9C2 and C2C12 myotubes via the My88-dependent TLR4 signaling pathway, Pharmaceutical Biology, 61:1, 1135-1151, DOI: 10.1080/13880209.2023.2230251

Abstract

Arjunolic acid (AA) is a triterpenoid saponin majorly found in the Terminalia arjuna and is claimed to exert the cardiovascular protective effects as a phytomedicine. However, it is unclear how AA exerts the effects at the molecular level. Hence, this study used an in vitro model using lipopolysaccharide (LPS)-stimulated H9C2 and C2C12 myotubes to investigate the cardioprotective effects of arjunolic acid (AA) via MyD88-dependant TLR4 downstream signaling markers expression. The myotubes were developed by differentiating rat H9C2 and mouse C2C12 myoblast cells. The MTT viability assay was used to assess the cytotoxicity of AA. LPS induced in vitro cardiovascular disease model was developed in H9C2 and C2C12 myotubes. The treatment groups were designed such as control (untreated), LPS control, positive control (LPS+ pyrrolidine dithiocarbamate (PDTC)-25 µM), and treatment groups were co-treated with LPS and three doses of AA (50, 75, and 100 µM). The changes in the expression of TLR4 downstream signaling markers were evaluated through High Content Screening (HCS) and Western Blot (WB) analysis. The outcomes demonstrated that the expression of MyD88, MAPK, JNK, and NFκB markers were significantly upregulated in the LPS-treated groups compared to the untreated control. Evidently, the HCS analysis revealed that MyD88, NF-κB, p38, and JNK were significantly downregulated in the H9C2 myotube in the AA treated groups (50, 75, and 100 µM). For, the C2C12 myotube, the expression of NFκB was downregulated. TLR4 marker expression in H9C2 and C2C12 myotubes was subsequently decreased by AA treatment, suggesting possible cardioprotective effects of AA.

Keywords

TLR4 signaling; H9C2 Myotube; C2C12 Myotube; Skeletal Muscle Cell; Cardiovascular disease; High Content Screening; MyD88

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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