Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes
High glucose-induced inflammation leads to atherosclerosis, which is considered a major cause of death in type 1 and type 2 diabetic patients. Nuclear factor-kappa B (NF-κB) plays a central role in high glucose-induced inflammation and is activated through toll-like receptors (TLRs) as well as canon...
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MDPI AG
2020-05-01
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| Series: | Molecules |
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| Online Access: | https://www.mdpi.com/1420-3049/25/10/2342 |
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| author | Eun Seong Jo Nipin Sp Dong Young Kang Alexis Rugamba Il Ho Kim Se Won Bae Qing Liu Kyoung-Jin Jang Young Mok Yang |
| author_facet | Eun Seong Jo Nipin Sp Dong Young Kang Alexis Rugamba Il Ho Kim Se Won Bae Qing Liu Kyoung-Jin Jang Young Mok Yang |
| author_sort | Eun Seong Jo |
| collection | DOAJ |
| description | High glucose-induced inflammation leads to atherosclerosis, which is considered a major cause of death in type 1 and type 2 diabetic patients. Nuclear factor-kappa B (NF-κB) plays a central role in high glucose-induced inflammation and is activated through toll-like receptors (TLRs) as well as canonical and protein kinase C-dependent (PKC) pathways. Non-toxic sulfur (NTS) and methylsulfonylmethane (MSM) are two sulfur-containing natural compounds that can induce anti-inflammation. Using Western blotting, real-time polymerase chain reaction, and flow cytometry, we found that high glucose-induced inflammation occurs through activation of TLRs. An effect of NTS and MSM on canonical and PKC-dependent NF-κB pathways was also demonstrated by western blotting. The effects of proinflammatory cytokines were investigated using a chromatin immunoprecipitation assay and enzyme-linked immunosorbent assay. Our results showed inhibition of the glucose-induced expression of TLR2 and TLR4 by NTS and MSM. These sulfur compounds also inhibited NF-κB activity through reactive oxygen species (ROS)-mediated canonical and PKC-dependent pathways. Finally, NTS and MSM inhibited the high glucose-induced expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and binding of NF-κB protein to the DNA of proinflammatory cytokines. Together, these results suggest that NTS and MSM may be potential drug candidates for anti-inflammation therapy. |
| first_indexed | 2024-03-10T19:46:17Z |
| format | Article |
| id | doaj.art-05be68cdffe64f5db5f21feff0f2ef3e |
| institution | Directory Open Access Journal |
| issn | 1420-3049 |
| language | English |
| last_indexed | 2024-03-10T19:46:17Z |
| publishDate | 2020-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Molecules |
| spelling | doaj.art-05be68cdffe64f5db5f21feff0f2ef3e2023-11-20T00:45:18ZengMDPI AGMolecules1420-30492020-05-012510234210.3390/molecules25102342Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human MonocytesEun Seong Jo0Nipin Sp1Dong Young Kang2Alexis Rugamba3Il Ho Kim4Se Won Bae5Qing Liu6Kyoung-Jin Jang7Young Mok Yang8Department of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaNara Bio Co., Ltd., Jeonju, North Jeolla 54852, KoreaGreen Chemistry & Materials Group, Korea Institute of Industrial Technology (KITECH), Cheonan 31056, KoreaJilin Green Food Engineering Research Institute, Changchun 130000, ChinaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaDepartment of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, KoreaHigh glucose-induced inflammation leads to atherosclerosis, which is considered a major cause of death in type 1 and type 2 diabetic patients. Nuclear factor-kappa B (NF-κB) plays a central role in high glucose-induced inflammation and is activated through toll-like receptors (TLRs) as well as canonical and protein kinase C-dependent (PKC) pathways. Non-toxic sulfur (NTS) and methylsulfonylmethane (MSM) are two sulfur-containing natural compounds that can induce anti-inflammation. Using Western blotting, real-time polymerase chain reaction, and flow cytometry, we found that high glucose-induced inflammation occurs through activation of TLRs. An effect of NTS and MSM on canonical and PKC-dependent NF-κB pathways was also demonstrated by western blotting. The effects of proinflammatory cytokines were investigated using a chromatin immunoprecipitation assay and enzyme-linked immunosorbent assay. Our results showed inhibition of the glucose-induced expression of TLR2 and TLR4 by NTS and MSM. These sulfur compounds also inhibited NF-κB activity through reactive oxygen species (ROS)-mediated canonical and PKC-dependent pathways. Finally, NTS and MSM inhibited the high glucose-induced expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and binding of NF-κB protein to the DNA of proinflammatory cytokines. Together, these results suggest that NTS and MSM may be potential drug candidates for anti-inflammation therapy.https://www.mdpi.com/1420-3049/25/10/2342High glucoseDiabetesTLRsNF-κBCanonical pathwayPKC pathway |
| spellingShingle | Eun Seong Jo Nipin Sp Dong Young Kang Alexis Rugamba Il Ho Kim Se Won Bae Qing Liu Kyoung-Jin Jang Young Mok Yang Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes Molecules High glucose Diabetes TLRs NF-κB Canonical pathway PKC pathway |
| title | Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes |
| title_full | Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes |
| title_fullStr | Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes |
| title_full_unstemmed | Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes |
| title_short | Sulfur Compounds Inhibit High Glucose-Induced Inflammation by Regulating NF-κB Signaling in Human Monocytes |
| title_sort | sulfur compounds inhibit high glucose induced inflammation by regulating nf κb signaling in human monocytes |
| topic | High glucose Diabetes TLRs NF-κB Canonical pathway PKC pathway |
| url | https://www.mdpi.com/1420-3049/25/10/2342 |
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