BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice
<b>Background/Objectives</b>: Degenerative arthritis is a chronic inflammatory disease marked by tissue degradation and vascular fibrosis. Macrophages play a central role in the inflammatory response by releasing mediators such as nitric oxide (NO), interleukin (IL)-6, tumor necrosis fac...
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2025-06-01
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| author | Joonpyo Hong Jin-Ho Lee Ga Young Lee Jin-Hwan Oh Hana Lee Han Sung Kim Tack-Joong Kim |
| author_facet | Joonpyo Hong Jin-Ho Lee Ga Young Lee Jin-Hwan Oh Hana Lee Han Sung Kim Tack-Joong Kim |
| author_sort | Joonpyo Hong |
| collection | DOAJ |
| description | <b>Background/Objectives</b>: Degenerative arthritis is a chronic inflammatory disease marked by tissue degradation and vascular fibrosis. Macrophages play a central role in the inflammatory response by releasing mediators such as nitric oxide (NO), interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), and prostaglandin E2 (PGE2). This study aimed to investigate the anti-inflammatory potential of BTEX-K, a formulation of dried red ginseng combined with alpha-galactosidase, in lipopolysaccharide (LPS)-stimulated cells. <b>Methods</b>: LPS-treated immune cells were used to assess the anti-inflammatory effects of BTEX-K. The levels of NO, IL-6, TNF-α, and PGE2 were measured following BTEX-K treatment. The protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was evaluated. Cytotoxicity assays were conducted to determine whether the observed effects were due to cell viability loss. The involvement of MAPK signaling and NF-κB pathway modulation was examined by analyzing JNK phosphorylation, IκB degradation, and PPAR-γ expression. <b>Results</b>: BTEX-K significantly reduced the production of NO, IL-6, TNF-α, and PGE2 in LPS-treated cells without inducing cytotoxicity. The protein expression levels of iNOS and COX-2 were also suppressed. Furthermore, BTEX-K inhibited the LPS-induced phosphorylation of JNK in the MAPK pathway. It restored IκB levels and suppressed NF-κB activation by preventing the downregulation of PPAR-γ. <b>Conclusions</b>: BTEX-K demonstrates notable anti-inflammatory effects by inhibiting key inflammatory mediators and signaling pathways in immune cells. These findings support its therapeutic potential in mitigating inflammation-related symptoms, including pain, swelling, and redness, commonly seen in degenerative arthritis. |
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| institution | Kabale University |
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| language | English |
| publishDate | 2025-06-01 |
| publisher | MDPI AG |
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| series | Biomedicines |
| spelling | doaj-art-b7be3f8b284d4e399a51b8053a1c6ebf2025-08-20T03:36:34ZengMDPI AGBiomedicines2227-90592025-06-01137152410.3390/biomedicines13071524BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis MiceJoonpyo Hong0Jin-Ho Lee1Ga Young Lee2Jin-Hwan Oh3Hana Lee4Han Sung Kim5Tack-Joong Kim6Division of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of KoreaCentral Research Institute, BTGin Co., Ltd., Deajeon 34024, Republic of KoreaCentral Research Institute, BTGin Co., Ltd., Deajeon 34024, Republic of KoreaDepartment of Biomedical Engineering, Yonsei University, Wonju 26493, Republic of KoreaDepartment of Biomedical Engineering, Yonsei University, Wonju 26493, Republic of KoreaDivision of Biological Science and Technology, Yonsei University, Wonju 26493, Republic of Korea<b>Background/Objectives</b>: Degenerative arthritis is a chronic inflammatory disease marked by tissue degradation and vascular fibrosis. Macrophages play a central role in the inflammatory response by releasing mediators such as nitric oxide (NO), interleukin (IL)-6, tumor necrosis factor alpha (TNF-α), and prostaglandin E2 (PGE2). This study aimed to investigate the anti-inflammatory potential of BTEX-K, a formulation of dried red ginseng combined with alpha-galactosidase, in lipopolysaccharide (LPS)-stimulated cells. <b>Methods</b>: LPS-treated immune cells were used to assess the anti-inflammatory effects of BTEX-K. The levels of NO, IL-6, TNF-α, and PGE2 were measured following BTEX-K treatment. The protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was evaluated. Cytotoxicity assays were conducted to determine whether the observed effects were due to cell viability loss. The involvement of MAPK signaling and NF-κB pathway modulation was examined by analyzing JNK phosphorylation, IκB degradation, and PPAR-γ expression. <b>Results</b>: BTEX-K significantly reduced the production of NO, IL-6, TNF-α, and PGE2 in LPS-treated cells without inducing cytotoxicity. The protein expression levels of iNOS and COX-2 were also suppressed. Furthermore, BTEX-K inhibited the LPS-induced phosphorylation of JNK in the MAPK pathway. It restored IκB levels and suppressed NF-κB activation by preventing the downregulation of PPAR-γ. <b>Conclusions</b>: BTEX-K demonstrates notable anti-inflammatory effects by inhibiting key inflammatory mediators and signaling pathways in immune cells. These findings support its therapeutic potential in mitigating inflammation-related symptoms, including pain, swelling, and redness, commonly seen in degenerative arthritis.https://www.mdpi.com/2227-9059/13/7/1524dried red ginsengBTEX-Kpro-inflammatory cytokinesnitric oxideMAPK pathwaychronic inflammation |
| spellingShingle | Joonpyo Hong Jin-Ho Lee Ga Young Lee Jin-Hwan Oh Hana Lee Han Sung Kim Tack-Joong Kim BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice Biomedicines dried red ginseng BTEX-K pro-inflammatory cytokines nitric oxide MAPK pathway chronic inflammation |
| title | BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice |
| title_full | BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice |
| title_fullStr | BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice |
| title_full_unstemmed | BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice |
| title_short | BTEX-K Ameliorates Rheumatoid Arthritis Through Regulating the NF-κB and PPAR-γ Signaling Pathways in Incomplete Freund’s Adjuvant-Induced Arthritis Mice |
| title_sort | btex k ameliorates rheumatoid arthritis through regulating the nf κb and ppar γ signaling pathways in incomplete freund s adjuvant induced arthritis mice |
| topic | dried red ginseng BTEX-K pro-inflammatory cytokines nitric oxide MAPK pathway chronic inflammation |
| url | https://www.mdpi.com/2227-9059/13/7/1524 |
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