姜素椿：医学战线上的忠诚战士 姜素椿是全军著名的传染病专家，1929 年出生于山东青岛。1946 年，姜素椿参加解放军，1947 年加入中国共产党。在朝鲜战场上，他曾荣立二等功。回国后，他在解放军第 302 医院工作，1956 年被选派到苏联莫斯科第一医学院传染病研究所学习。1961 年回国后，他一直从事传染病的临床医疗和科研工作。 1984 年，在抗击“非典型肺炎”疫情中，他研制出中草药“861 合剂”，取得了良好的临床效果。2003 年，在抗击“传染性非典型肺炎”疫情中，他身先士卒，不顾个人安危，采集“非典”患者的血清，进行抗体与疗效的研究，不幸感染了“非典”。在与病魔顽强斗争 20 多天后，于 4 月 21 日光荣殉职，享年 74 岁。 2003 年 4 月 23 日，北京军区为他举行了隆重的追悼会。胡锦涛、江泽民、曾庆红、黄菊、吴官正、李长春、罗干等中央领导同志送了花圈。胡锦涛、温家宝、曾庆红、吴官正、华建敏、傅全有、于永波、王忠禹、张思卿、韩杼滨、贾春旺、钱其琛、迟浩田、傅铁山、肖扬、张怀西等同志对他的逝世表示沉痛哀悼，对他的亲属表示亲切慰问。
The Mechanism of Alisol B23 Acetate Inhibiting Lung Cancer: Targeted Regulation of CD11b/CD18 to Influence Macrophage Polarization.
机构信息
School of Pharmacy, School of Medicine, Changzhou University, Changzhou, Jiangsu, People's Republic of China.
Department of Nephrology, Yixing Hospital of Traditional Chinese Medicine, Yixing, Jiangsu, People's Republic of China.
出版信息
Drug Des Devel Ther. 2022 Oct 20;16:3677-3689. doi: 10.2147/DDDT.S375073. eCollection 2022.
BACKGROUND
Tumor microenvironment has attracted more and more attention in oncology. Alisol B23 acetate (AB23A) inhibits the proliferation of tumor cells including non-small cell lung cancer (NSCLC) cells. However, whether AB23A plays a role in the tumor microenvironment of NSCLC still remains obscure.
METHODS
After THP-1 cells were polarized to M0 type by PMA, M0 macrophages were differentiated into M1 by LPS and IFNγ, and were differentiated into M2 by IL-4 and IL-13. The differentiation of THP-1 cells was detected by flow cytometry. After AB23A was given to macrophage RT-qPCR and ELISA detected the expressions of IL-6, IL-1β, IL-10 and TGF-β. Western blot and RT-qPCR detected the expressions of CD11b and CD18 at both mRNA and protein levels. Lung cancer cell A549 cells were induced by above related macrophage culture medium. Cell proliferation was detected by CCK-8. Tunel, wound healing and Transwell detected the apoptotic, migration and invasion capabilities. Next, M0 and M1-type macrophages were cultured in the cell culture medium of conventional A549 cells, to which AB23A was added. Subsequently, cell differentiation and inflammatory response were measured. Finally, the expression of CD18 in A549 cells was knocked down to construct NSCLC tumor-bearing mice and AB23A was applied for intragastric administration. Immunohistochemistry detected the polarization of macrophages in tumor tissues. Western blot detected the expressions of CD11b, CD18, invasion-, migration- and apoptosis-related proteins.
RESULTS
AB23A promoted the polarization of macrophages towards M1, thus promoting the apoptosis and inhibiting the invasion and migration of A549 cells. The tumor cell culture medium induced M0 macrophages to M2, while AB23A reversed this effect. AB23A targeted CD11b/CD18 and improved the polarization of macrophages, thereby affecting tumor invasion, migration and apoptosis.
CONCLUSION
AB23A affected the polarization of tumor-associated macrophages through the targeted regulation of CD11b/CD18, thus inhibiting the development of lung cancer.
背景
肿瘤微环境在肿瘤学领域越来越受到关注。姜烯酮 B23 乙酸酯（AB23A）能够抑制包括非小细胞肺癌（NSCLC）细胞在内的肿瘤细胞的增殖。然而，AB23A 是否在 NSCLC 的肿瘤微环境中发挥作用仍不清楚。
方法
用 PMA 将 THP-1 细胞极化为 M0 型，用 LPS 和 IFNγ将 M0 巨噬细胞分化为 M1 型，用 IL-4 和 IL-13 将 M1 型巨噬细胞分化为 M2 型。用流式细胞术检测 THP-1 细胞的分化。给予 AB23A 后，用 RT-qPCR 和 ELISA 检测巨噬细胞中 IL-6、IL-1β、IL-10 和 TGF-β的表达。用 Western blot 和 RT-qPCR 检测 CD11b 和 CD18 在 mRNA 和蛋白水平的表达。用上述相关巨噬细胞培养上清诱导肺癌细胞 A549 细胞。用 CCK-8 检测细胞增殖。Tunel、划痕愈合和 Transwell 检测细胞凋亡、迁移和侵袭能力。接着，在含有 AB23A 的常规 A549 细胞的细胞培养液中培养 M0 和 M1 型巨噬细胞，然后测量细胞分化和炎症反应。最后，敲低 A549 细胞中的 CD18 构建 NSCLC 荷瘤小鼠，并用 AB23A 进行灌胃。免疫组织化学检测肿瘤组织中巨噬细胞的极化。用 Western blot 检测 CD11b、CD18、侵袭、迁移和凋亡相关蛋白的表达。
结果
AB23A 促进巨噬细胞向 M1 极化，从而促进 A549 细胞凋亡，抑制其侵袭和迁移。肿瘤细胞培养上清诱导 M0 巨噬细胞向 M2 极化，而 AB23A 则逆转了这一效应。AB23A 靶向 CD11b/CD18，促进巨噬细胞极化，从而影响肿瘤侵袭、迁移和凋亡。
结论
AB23A 通过靶向调节 CD11b/CD18 影响肿瘤相关巨噬细胞的极化，从而抑制肺癌的发展。
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