2024年5月20日，武汉大学中南医院循证与转化医学中心，Jiao Huang, Cheng Fang，Shuang Ying Wang等老师在Military Medical Research（IF=21.1）上，在线发表题为“P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway”的论文，此论文使用了联科生物Annexin V-APC/PI Apoptosis Kit（货号：AP107）、Cell Cycle Staining Kit 细胞周期检测试剂盒(货号：CCS012）这两个产品。
P. gingivalis LPS decreased apoptosis of WPMY-1 cells and increased cell growth. a Flow cytometry apoptotic representative images and apoptosis rate histogram of WPMY-1 cells treated with selected concentrations of 0, 0.1 and 1 μg/ml P.g-LPS for 24 h. b Flow cytometry representative images and quantitative analyses of cell cycle of WPMY-1 cells treated with selected concentrations of 0, 0.1 and 1 μg/ml P.g-LPS for 24 h.
研究发现在患有良性前列腺增生合并牙周炎的患者的精液和前列腺液中，同时检测到了牙龈卟啉单胞菌（P. g）、口腔链球菌（Streptococcus oralis）、橙黄褐杆菌（Capnocytophaga ochracea）和其他口腔病原体，并且发现P. g的平均相对丰度最高。在62.5%的患者中，P. g在精液和前列腺液中均被检测到，牙周炎和良性前列腺增生同时发生会加剧前列腺的组织学变化。
进一步实验研究发现牙龈卟啉单胞菌及其脂多糖（P.g-LPS）感染可明显引起前列腺上皮和基质的增生，并增加胶原纤维化。P. g感染促进了前列腺细胞的增殖，抑制了细胞凋亡，并上调了前列腺组织中炎症细胞因子白细胞介素-6（IL-6）、白细胞介素-6受体α（IL-6Rα）和糖蛋白130（gp130）的表达。P.g-LPS可显著抑制细胞凋亡，促进细胞有丝分裂和增殖，并且通过IL-6/IL-6Rα/gp130复合体激活Akt途径，破坏前列腺细胞增殖与凋亡之间的平衡，从而诱导良性前列腺增生的发生。联科试剂盒助力科研流式凋亡以及周期产品部分引用文献
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参考文献：Wang SY, Cai Y, Hu X, et al. P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway. Mil Med Res. 2024;11(1):30. Published 2024 May 20.
原文链接：https://link.springer.com/article/10.1186/s40779-024-00533-8
