Baicalin Reduces Lung Inflammation by Blocking Key Inflammatory Pathway

Jim Crocker
16th September, 2024

Baicalin Reduces Lung Inflammation by Blocking Key Inflammatory Pathway

Image Source: Natural Science News, 2024

Key Findings

  • The study from Guizhou Medical University found that baicalin reduces lung inflammation in acute lung injury (ALI) by inhibiting the NF-κB pathway
  • Baicalin significantly lowered the levels of inflammatory molecules and cytokines in human microvascular endothelial cells and in an ALI mouse model
  • The research suggests baicalin could be a potential therapeutic strategy for ALI by targeting specific inflammatory pathways
Acute lung injury (ALI) is a severe pulmonary condition characterized by damage to alveolar epithelial cells and microvascular endothelial cells, leading to respiratory distress and inflammation. A common pathological mechanism in ALI is the activation of the complement system, particularly the alternative pathway. A recent study conducted by Guizhou Medical University explored the interventional effects of baicalin, a flavonoid derived from the root of Scutellaria baicalensis Georgi, on microangiopathy in ALI induced by complement alternative pathway activation[1]. The study aimed to investigate how baicalin influences the inflammatory processes in ALI. The researchers activated the complement alternative pathway using cobra venom factor (CVF) and conducted experiments on human microvascular endothelial cells (HMEC). These cells were pretreated with baicalin before exposure to complement activation products. The expression of inflammatory mediators was detected using enzyme-linked immunosorbent assay (ELISA), and the intranuclear transcriptional activity of NF-κB was assessed using a dual fluorescent kinase reporter gene assay kit. Additionally, an ALI mouse model was established by injecting CVF into the tail vein, and baicalin or PDTC was administered to the mice for seven days prior to CVF injection. Pathological changes, complement activation product deposition, and NF-κB p65 phosphorylation in lung tissue were evaluated through HE staining and immunohistochemistry. The findings revealed that baicalin significantly reduced the expression of adhesion molecules (ICAM-1, VCAM-1, E-selectin) and cytokines (IL-6, TNF-α) in HMEC cells induced by complement alternative activation products. Baicalin also decreased the intranuclear transcriptional activity of NF-κB, a key regulator of inflammation. In the ALI mouse model, baicalin intervention led to a reduction in the number of inflammatory cells and protein content in bronchoalveolar lavage fluid (BALF), as well as decreased levels of IL-6, TNF-α, and ICAM-1 in serum and IL-6, TNF-α, ICAM-1, and P-selectin in BALF. Furthermore, baicalin attenuated inflammatory cell infiltration in lung tissue and reduced the deposition of complement activation products (C5a, C5b-9) and phosphorylation of NF-κB p65 in lung tissue. These results suggest that baicalin alleviates lung inflammation induced by complement alternative pathway activation by inhibiting the NF-κB pathway, thereby delaying the progression of ALI. This study provides new insights into potential therapeutic strategies for ALI, highlighting the importance of targeting specific inflammatory pathways to improve patient outcomes. This research aligns with previous studies that have identified the role of the complement system in ALI and ARDS. Complement activation can lead to a robust inflammatory response, causing significant lung damage[2]. In particular, the lectin pathway of complement has been shown to contribute to ARDS pathology, and its inhibition has been found to improve outcomes in experimental models[3]. The current study expands on these findings by demonstrating the therapeutic potential of baicalin in modulating the complement alternative pathway and reducing lung inflammation. The study also underscores the need for individualized treatment approaches in ALI and ARDS, as different subtypes of the conditions may respond differently to various therapies[4]. By targeting specific pathways involved in the inflammatory response, such as the NF-κB pathway in the case of baicalin, more effective and tailored treatments can be developed to improve patient survival and quality of life. In conclusion, the study conducted by Guizhou Medical University provides compelling evidence that baicalin can mitigate lung inflammation in ALI by inhibiting the NF-κB pathway. This research contributes to the growing body of knowledge on the role of the complement system in ALI and ARDS and suggests new avenues for therapeutic intervention.

MedicineHealthBiochem

References

Main Study

1) Baicalin relieves complement alternative pathway activation-induced lung inflammation through inhibition of NF-κB pathway.

Published 13th September, 2024

https://doi.org/10.1186/s12906-024-04622-y

Related Studies

2) Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.

https://doi.org/10.3389/fimmu.2023.1100461

3) Inhibition of the lectin pathway of complement activation reduces LPS-induced acute respiratory distress syndrome in mice.

https://doi.org/10.3389/fimmu.2023.1192767

4) Acute lung injury - from pathophysiology to treatment.

Journal: Physiological research, Issue: Vol 69, Issue Suppl 3, Dec 2020


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