Correction to "Diterpenoid Tanshinones Can Inhibit Lung Cancer Progression by Improving the Tumor Microenvironment and Downregulation of NF-κB Expression".

[This corrects the article DOI: 10.1021/acsomega.3c09667.].

Diterpenoid Tanshinones Can Inhibit Lung Cancer Progression by Improving the Tumor Microenvironment and Downregulation of NF-κB Expression.

Diterpenoid tanshinones (DTs) are a bioactive fraction extracted from Salvia miltiorrhiza. High-performance liquid chromatography analysis revealed the presence of four compounds, namely, tanshinone IIA, tanshinone I, cryptotanshinone, and dihydrotanshinone. In this study, we aimed to propose a possible mechanism for the anti-lung cancer effect of DT. To do so, we utilized a lung cancer nude mice model and a lung cancer cell line (PC9) to investigate the effect of DT on lung cancer. We employed immunohistochemistry, enzyme-linked immunosorbent assay, hematoxylin and eosin staining, and immunofluorescence to analyze the pharmacological role of DT in the inhibition of lung cancer growth. The results showed that DT inhibited tumor growth, induced apoptosis in the nude mice model, and reduced inflammatory cell infiltration. Additionally, DT inhibited PC9 lung cancer cells, growth, proliferation, and migration. The mechanism of action of DT involves not only directly inhibiting cell proliferation and migration but also improving the tumor microenvironment. DT significantly increased the expression of important intestinal gap junction proteins, such as zonula occludens 1 (ZO-1) and occludin I. This upregulation contributes to the reinforcement of the intestinal mucosal barrier, thereby reducing the paracellular transport of lipopolysaccharides (LPS) through the intestine. Consequently, the decreased LPS levels lead to the inhibition of NF-κB expression and downregulation of macrophage polarization, as indicated by the decreased expression of CD68. In conclusion, this study has confirmed that DT has anti-lung cancer properties by improving the inflammatory tumor microenvironment via regulating macrophage polarization and inhibiting LPS-associated immune response. These results provide new insights into the mechanism of DT action against lung cancer.

The landscape of pathophysiology guided therapeutic strategies for gout treatment.

INTRODUCTION: Gout is a common autoinflammatory disease caused by hyperuricemia with acute and/or chronic inflammation as well as tissue damage. Currently, urate-lowering therapy (ULT) and anti-inflammatory therapy are used as first-line strategies for gout treatment. However, traditional drugs for gout treatment exhibit some unexpected side effects and are not suitable for certain patients due to their comorbidity with other chronic disease. AREAS COVERED: In this review, we described the pathophysiology of hyperuricemia and monosodium urate (MSU) crystal induced inflammatory response during gout development in depth and comprehensively summarized the advances in the investigation of promising ULT drugs as well as anti-inflammatory drugs that might be safer and more effective for gout treatment. EXPERT OPINION: New drugs that are developed based on these molecular mechanisms exhibited great efficacy on reduction of disease burden both in vitro and in vivo, implying their potential for clinical application. Moreover, hyperthermia also showed regulation effect on MSU crystals formation and the signaling pathways involved in inflammation.