Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway
Osteoarthritis (OA) is a chronic degenerative joint disease characterized by the deterioration of articular cartilage. The progression of OA leads to an increase in inflammatory mediators in the joints, thereby promoting the destruction of the cartilage matrix. Recent studies have reported on the an...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-05-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/10/6/862 |
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| author | Yi-Jen Peng Jeng-Wei Lu Chian-Her Lee Herng-Sheng Lee You-Hsiang Chu Yi-Jung Ho Feng-Cheng Liu Chun-Jung Huang Chia-Chun Wu Chih-Chien Wang |
| author_facet | Yi-Jen Peng Jeng-Wei Lu Chian-Her Lee Herng-Sheng Lee You-Hsiang Chu Yi-Jung Ho Feng-Cheng Liu Chun-Jung Huang Chia-Chun Wu Chih-Chien Wang |
| author_sort | Yi-Jen Peng |
| collection | DOAJ |
| description | Osteoarthritis (OA) is a chronic degenerative joint disease characterized by the deterioration of articular cartilage. The progression of OA leads to an increase in inflammatory mediators in the joints, thereby promoting the destruction of the cartilage matrix. Recent studies have reported on the anti-inflammatory and antioxidant properties of cardamonin, which also appears to interact with cellular targets, such as nuclear erythroid 2-related factor 2 (Nrf2), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) during the progression of tumors. To date, few studies have investigated the effects of cardamonin on chondrocyte inflammation. In the current study, we determined that treating interleukin-1 beta (IL-1β-stimulated chondrocyte cells) with cardamonin significantly reduced the release of nitric oxide (NO) and prostaglandin E2 (PGE2) and significantly inhibited the expression of pro-inflammatory proteins, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Cardamonin was also shown to: (1) inhibit the activation and production of matrix metalloproteinases (MMPs), (2) suppress the nuclear factor-κB (NF-κB) signaling pathway, (3) suppress the expression of toll-like receptor proteins, (4) activate the Nrf2 signaling pathway, and (5) increase the levels of antioxidant proteins heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The increase in antioxidant proteins led to corresponding antioxidant effects (which were abolished by Nrf2 siRNA). Our findings identify cardamonin as a candidate Nrf2 activator for the treatment and prevention of OA related to inflammation and oxidative stress. |
| first_indexed | 2024-03-10T10:58:44Z |
| format | Article |
| id | doaj.art-9ab98c7d5f1043798b38fd003e0326aa |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T10:58:44Z |
| publishDate | 2021-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-9ab98c7d5f1043798b38fd003e0326aa2023-11-21T21:41:13ZengMDPI AGAntioxidants2076-39212021-05-0110686210.3390/antiox10060862Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 PathwayYi-Jen Peng0Jeng-Wei Lu1Chian-Her Lee2Herng-Sheng Lee3You-Hsiang Chu4Yi-Jung Ho5Feng-Cheng Liu6Chun-Jung Huang7Chia-Chun Wu8Chih-Chien Wang9Department of Pathology, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, TaiwanDepartment of Biological Sciences, National University of Singapore, Singapore 117543, SingaporeDepartment of Orthopedics, School of Medicine, College of Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei 110, TaiwanLaboratory Medicine, Department of Pathology, Kaohsiung Veterans General Hospital, Kaohsiung 813, TaiwanNational Defense Medical Center, Graduate Institute of Life Sciences, Taipei 114, TaiwanNational Defense Medical Center, Graduate Institute of Life Sciences, Taipei 114, TaiwanDepartment of Medicine, Rheumatology/Immunology and Allergy, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, TaiwanDepartment of Pathology, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, TaiwanDepartment of Orthopedics, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, TaiwanDepartment of Orthopedics, National Defense Medical Center, Tri-Service General Hospital, Taipei 114, TaiwanOsteoarthritis (OA) is a chronic degenerative joint disease characterized by the deterioration of articular cartilage. The progression of OA leads to an increase in inflammatory mediators in the joints, thereby promoting the destruction of the cartilage matrix. Recent studies have reported on the anti-inflammatory and antioxidant properties of cardamonin, which also appears to interact with cellular targets, such as nuclear erythroid 2-related factor 2 (Nrf2), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) during the progression of tumors. To date, few studies have investigated the effects of cardamonin on chondrocyte inflammation. In the current study, we determined that treating interleukin-1 beta (IL-1β-stimulated chondrocyte cells) with cardamonin significantly reduced the release of nitric oxide (NO) and prostaglandin E2 (PGE2) and significantly inhibited the expression of pro-inflammatory proteins, including inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2). Cardamonin was also shown to: (1) inhibit the activation and production of matrix metalloproteinases (MMPs), (2) suppress the nuclear factor-κB (NF-κB) signaling pathway, (3) suppress the expression of toll-like receptor proteins, (4) activate the Nrf2 signaling pathway, and (5) increase the levels of antioxidant proteins heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The increase in antioxidant proteins led to corresponding antioxidant effects (which were abolished by Nrf2 siRNA). Our findings identify cardamonin as a candidate Nrf2 activator for the treatment and prevention of OA related to inflammation and oxidative stress.https://www.mdpi.com/2076-3921/10/6/862osteoarthritiscardamoninoxidative stresschondrocyteinterleukin-1 beta |
| spellingShingle | Yi-Jen Peng Jeng-Wei Lu Chian-Her Lee Herng-Sheng Lee You-Hsiang Chu Yi-Jung Ho Feng-Cheng Liu Chun-Jung Huang Chia-Chun Wu Chih-Chien Wang Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway Antioxidants osteoarthritis cardamonin oxidative stress chondrocyte interleukin-1 beta |
| title | Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway |
| title_full | Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway |
| title_fullStr | Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway |
| title_full_unstemmed | Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway |
| title_short | Cardamonin Attenuates Inflammation and Oxidative Stress in Interleukin-1β-Stimulated Osteoarthritis Chondrocyte through the Nrf2 Pathway |
| title_sort | cardamonin attenuates inflammation and oxidative stress in interleukin 1β stimulated osteoarthritis chondrocyte through the nrf2 pathway |
| topic | osteoarthritis cardamonin oxidative stress chondrocyte interleukin-1 beta |
| url | https://www.mdpi.com/2076-3921/10/6/862 |
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