Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways

Apigetrin is a glycosidic flavonoid derived from <i>Teucrium gnaphalodes</i> that has a wide range of biological activities, including antioxidant, anti-inflammatory, and anticancer. Inflammation is a kind of defense mechanism in the body. Flavonoids are natural phytochemicals that exert...

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Main Authors: Sang-Eun Ha, Pritam Bhagwan Bhosale, Hun-Hwan Kim, Min-Yeong Park, Abuyaseer Abusaliya, Gon-Sup Kim, Jin-A Kim
Format: Article
Language:English
Published: MDPI AG 2022-06-01
Series:Current Issues in Molecular Biology
Subjects:
Online Access:https://www.mdpi.com/1467-3045/44/6/180
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author Sang-Eun Ha
Pritam Bhagwan Bhosale
Hun-Hwan Kim
Min-Yeong Park
Abuyaseer Abusaliya
Gon-Sup Kim
Jin-A Kim
author_facet Sang-Eun Ha
Pritam Bhagwan Bhosale
Hun-Hwan Kim
Min-Yeong Park
Abuyaseer Abusaliya
Gon-Sup Kim
Jin-A Kim
author_sort Sang-Eun Ha
collection DOAJ
description Apigetrin is a glycosidic flavonoid derived from <i>Teucrium gnaphalodes</i> that has a wide range of biological activities, including antioxidant, anti-inflammatory, and anticancer. Inflammation is a kind of defense mechanism in the body. Flavonoids are natural phytochemicals that exert anti-inflammatory effects in numerous cells. In the present study, we investigated the anti-inflammatory effect of apigetrin and its underlying mechanism of activity in skeletal muscle cells (L6). The determination of cytotoxicity was performed by MTT assay. We treated L6 cells with apigetrin, and nontoxic concentrations were chosen to perform further experimentation. Apigetrin inhibited the expression of iNOS and COX-2 induced by LPS in a dose-dependent manner. iNOS and COX-2 are inflammatory markers responsible for enhancing the inflammatory response. Apigetrin also inhibited the LPS-induced phosphorylation of p65 and IκB-α. NF-κB signaling regulates the inflammatory process by mediating various proinflammatory genes. Similarly, the MAPK signaling pathway consists of ERK, JNK, and p38, which plays a critical role in the production of cytokines and downstream signaling events leading to inflammation. Apigetrin significantly downregulated the phosphorylation of JNK and p38, but did not affect the phosphorylation of ERK in the LPS-stimulated cells. These findings indicate the correlation between the anti-inflammatory activity of NF-κB and the MAPK signaling pathway. Thus, our overall finding suggests that apigetrin has anti-inflammatory effects and it can be considered for further drug design on L6 skeletal muscle cells.
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spelling doaj.art-4046ddab682a402ea4c95ac504710ce22023-12-01T23:14:53ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452022-06-014462635264510.3390/cimb44060180Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling PathwaysSang-Eun Ha0Pritam Bhagwan Bhosale1Hun-Hwan Kim2Min-Yeong Park3Abuyaseer Abusaliya4Gon-Sup Kim5Jin-A Kim6Research Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaResearch Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaResearch Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaResearch Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaResearch Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaResearch Institute of Life Science, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, KoreaDepartment of Physical Therapy, International University of Korea, Jinju 52833, KoreaApigetrin is a glycosidic flavonoid derived from <i>Teucrium gnaphalodes</i> that has a wide range of biological activities, including antioxidant, anti-inflammatory, and anticancer. Inflammation is a kind of defense mechanism in the body. Flavonoids are natural phytochemicals that exert anti-inflammatory effects in numerous cells. In the present study, we investigated the anti-inflammatory effect of apigetrin and its underlying mechanism of activity in skeletal muscle cells (L6). The determination of cytotoxicity was performed by MTT assay. We treated L6 cells with apigetrin, and nontoxic concentrations were chosen to perform further experimentation. Apigetrin inhibited the expression of iNOS and COX-2 induced by LPS in a dose-dependent manner. iNOS and COX-2 are inflammatory markers responsible for enhancing the inflammatory response. Apigetrin also inhibited the LPS-induced phosphorylation of p65 and IκB-α. NF-κB signaling regulates the inflammatory process by mediating various proinflammatory genes. Similarly, the MAPK signaling pathway consists of ERK, JNK, and p38, which plays a critical role in the production of cytokines and downstream signaling events leading to inflammation. Apigetrin significantly downregulated the phosphorylation of JNK and p38, but did not affect the phosphorylation of ERK in the LPS-stimulated cells. These findings indicate the correlation between the anti-inflammatory activity of NF-κB and the MAPK signaling pathway. Thus, our overall finding suggests that apigetrin has anti-inflammatory effects and it can be considered for further drug design on L6 skeletal muscle cells.https://www.mdpi.com/1467-3045/44/6/180apigetrinL6anti-inflammationNF-κBMAPK
spellingShingle Sang-Eun Ha
Pritam Bhagwan Bhosale
Hun-Hwan Kim
Min-Yeong Park
Abuyaseer Abusaliya
Gon-Sup Kim
Jin-A Kim
Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
Current Issues in Molecular Biology
apigetrin
L6
anti-inflammation
NF-κB
MAPK
title Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
title_full Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
title_fullStr Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
title_full_unstemmed Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
title_short Apigetrin Abrogates Lipopolysaccharide-Induced Inflammation in L6 Skeletal Muscle Cells through NF-κB/MAPK Signaling Pathways
title_sort apigetrin abrogates lipopolysaccharide induced inflammation in l6 skeletal muscle cells through nf κb mapk signaling pathways
topic apigetrin
L6
anti-inflammation
NF-κB
MAPK
url https://www.mdpi.com/1467-3045/44/6/180
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