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Gao, Long, Davtyan, Nara, Zhang, Ruiyong. (1405). Rhein Confers Protection Against Pneumococcal Pneumonia via Immunomodulation of the MAPK/NF-κB Axis. سامانه مدیریت نشریات علمی, 23(2), 6-6. doi: 10.22034/iji.2026.109529.3138
Long Gao; Nara Davtyan; Ruiyong Zhang. "Rhein Confers Protection Against Pneumococcal Pneumonia via Immunomodulation of the MAPK/NF-κB Axis". سامانه مدیریت نشریات علمی, 23, 2, 1405, 6-6. doi: 10.22034/iji.2026.109529.3138
Gao, Long, Davtyan, Nara, Zhang, Ruiyong. (1405). 'Rhein Confers Protection Against Pneumococcal Pneumonia via Immunomodulation of the MAPK/NF-κB Axis', سامانه مدیریت نشریات علمی, 23(2), pp. 6-6. doi: 10.22034/iji.2026.109529.3138
Gao, Long, Davtyan, Nara, Zhang, Ruiyong. Rhein Confers Protection Against Pneumococcal Pneumonia via Immunomodulation of the MAPK/NF-κB Axis. سامانه مدیریت نشریات علمی, 1405; 23(2): 6-6. doi: 10.22034/iji.2026.109529.3138

Rhein Confers Protection Against Pneumococcal Pneumonia via Immunomodulation of the MAPK/NF-κB Axis

Iranian Journal of Immunology
دوره 23، شماره 2، شهریور 2026، صفحه 6-6
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22034/iji.2026.109529.3138
نویسندگان
Long Gao1؛ Nara Davtyan2؛ Ruiyong Zhang* 3
1Department of Emergency Medicine, Traditional Chinese Medicine Hospital of Baoji, Baoji,721004, China
2Yerevan State University, Yerevan, Armenia
3Department of Otolaryngology, Traditional Chinese Medicine Hospital of Baoji, Baoji，721004, China
چکیده
Background: Streptococcus pneumoniae remains a leading cause of community-acquired pneumonia. Severe pulmonary inflammation and subsequent tissue damage are driven significantly by the overexpression of both the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Mitogen-Activated Protein Kinase (MAPK) signaling pathways.
Objective: To investigate the immunomodulatory effects of rhein in a mouse model of Streptococcus pneumoniae-induced pneumonia .
Methods: Forty male C57BL/6 mice were randomly assigned to four experimental groups: healthy control, S. pneumoniae infected control, and two rhein-treatment groups (10 mg/kg and 30 mg/kg). Expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-10, transforming growth factor (TGF)-β, monocyte chemoattractant protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) in lung tissues and bronchoalveolar lavage fluid (BALF) were quantified using reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Additionally, ELISA and Western blotting were employed to assess the phosphorylation profiles of MAPK and NF-κB.
Results: Rhein significantly decreased the lung wet/dry weight ratio, reduced bacterial load, and downregulated COX-2 and iNOS expression. Cytokine analysis revealed marked reductions in pro-inflammatory mediators (IL-6, IL-1β, TNF-α, and MCP-1) alongside elevated levels of the anti-inflammatory cytokine IL-10 in both lung tissues and BALF. Furthermore, ELISA and Western blotting confirmed that rhein significantly inhibited the phosphorylation of MAPK and NF-κB.
Conclusion: Rhein attenuates S. pneumoniae-induced pulmonary inflammation and injury by modulating the MAPK/NF-κB signaling pathways. These findings highlight Rhein as a promising potential therapeutic agent for pneumococcal pneumonia and related inflammatory lung diseases.
کلیدواژه‌ها
S. pneumoniae؛ Immunomodulatory؛ Therapeutic agent؛ Cytokine
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