Abstract

Introduction: Alveolar macrophages (AM) are involved in the development and progression of a variety of lung diseases. It is of great significance to explore the pathogenesis of diseases and evaluate the efficacy of drugs. However, there is no standard process for extracting primary AM. Nitidine chloride is an alkaloid extracted from Zanthoxylum nitidum (Roxb.) DC., which has an anti-tumour pharmacological effect. However, there is no evidence that nitidine chloride has a direct effect on CRC cell lung metastasis. The purpose of this study was to establish a standard for the extraction of primary AM from mice and to investigate the pharmacodynamics of nitidine chloride in mice with lung metastases to colorectal cancer. Methods: The standard for the extraction of mouse primary AM by lavage was established. Western blot and PCR were used to detect the regulatory mechanism of nitidine chloride in the treatment of lung metastasis in mice by macrophage phenotype and glycolysis level. Results: The results showed that sufficient quantity and quality of primary AM could be obtained by optimising extraction steps, and AM obtained by this method could accurately reflect disease progression. At the same time, nitidine chloride can effectively reduce colorectal cancer lung metastasis in mice. From the mechanism, nitidine chloride can inhibit the expression of M2 macrophage markers and the levels of mRNA and proteins of the glycolysis-limiting enzyme. Conclusions: Our results show that primary AM that accurately reflect disease and assess pharmacological effects can be obtained using our established criteria. The inhibitory effect of nitidine chloride on colorectal cancer lung metastasis may be attributed to its regulation of macrophage phenotype and glycolysis.

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