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This research investigates the effects of rhein on pneumonia caused by Streptococcus pneumoniae in a mouse model.

June 30, 20260 citations

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

LGLong GaoBaoji City Central Hospital NDNara DavtyanYerevan State University RZRuiyong ZhangBaoji City Central Hospital

Key Points

This research investigates the effects of rhein on pneumonia caused by Streptococcus pneumoniae in a mouse model.
Forty male C57BL/6 mice were randomly assigned to four groups: healthy control, infected control, and two rhein treatment groups.
Quantitative assessments of inflammatory markers and signaling pathway activation were performed using RT-PCR, ELISA, and Western blotting.
Doses of rhein were administered at 10 mg/kg and 30 mg/kg to evaluate their effects.
Rhein significantly decreased the lung wet/dry weight ratio and bacterial load.
Pro-inflammatory mediators IL-6, IL-1β, TNF-α, and MCP-1 were markedly reduced, while IL-10 levels increased in lung tissues and BALF.
Rhein inhibited the phosphorylation of MAPK and NF-κB, showing its role in reducing inflammation.

Abstract

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.

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