2024年5月20日，武漢大學中南醫院循證與轉化醫學中心，Jiao Huang, Cheng Fang，Shuang Ying Wang等老師在Military Medical Research（IF=21.1）上，在線發表題為“P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway”的論文，此論文使用了聯科生物Annexin V-APC/PI Apoptosis Kit（貨號：AP107）、Cell Cycle Staining Kit 細胞周期檢測試劑盒(貨號：CCS012）這兩個產品。
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.
研究發現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，同時檢測到了牙齦卟啉單胞菌（P. g）、口腔鏈球菌（Streptococcus oralis）、橙黃褐桿菌（Capnocytophaga ochracea）和其他口腔病原體，并且發現P. g的平均相對豐度最高。在62.5%的患者中，P. g在精液和前列腺液中均被檢測到，牙周炎和良性前列腺增生同時發生會加劇前列腺的組織學變化。
進一步實驗研究發現牙齦卟啉單胞菌及其脂多糖（P.g-LPS）感染可明顯引起前列腺上皮和基質的增生，并增加膠原纖維化。P. g感染促進了前列腺細胞的增殖，抑制了細胞凋亡，并上調了前列腺組織中炎癥細胞因子白細胞介素-6（IL-6）、白細胞介素-6受體α（IL-6Rα）和糖蛋白130（gp130）的表達。P.g-LPS可顯著抑制細胞凋亡，促進細胞有絲分裂和增殖，并且通過IL-6/IL-6Rα/gp130復合體激活Akt途徑，破壞前列腺細胞增殖與凋亡之間的平衡，從而誘導良性前列腺增生的發生。聯科試劑盒助力科研流式凋亡以及周期產品部分引用文獻
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參考文獻：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.
原文鏈接：https://link.springer.com/article/10.1186/s40779-024-00533-8
