目的 研究氧化苦參堿（OM）對(duì)脂多糖（LPS）誘導(dǎo)的大鼠胰腺星狀細(xì)胞株（PSCs）NOD樣受體蛋白3（NLRP3）活化的影響。方法 通過(guò)設(shè)置不同劑量（0、2.5、5、10、20、40 μg/mL）的LPS并設(shè)置相同劑量（10 μg/mL）的LPS刺激LTC14細(xì)胞不同時(shí)間（0、1、3、6、9、12 h），利用Western blotting檢測(cè)技術(shù)，考察LPS引起炎性小體活化的量效關(guān)系；使用OM、Janus蛋白酪氨酸激酶2（JAK2）抑制劑AG490干預(yù)LPS誘導(dǎo)的LTC14細(xì)胞株后，通過(guò)Westernblotting技術(shù)檢測(cè)Janus蛋白酪氨酸激酶2/信號(hào)轉(zhuǎn)導(dǎo)子和轉(zhuǎn)錄激活子3（JAK2/STAT3）信號(hào)通路中相關(guān)分子以及NLRP3炎性小體相關(guān)蛋白表達(dá)的變化。結(jié)果 與對(duì)照組比較，LTC14細(xì)胞接受不同濃度的LPS刺激后JAK2、STAT3、NLRP3、caspase1、白細(xì)胞介素-1β（IL-1β）蛋白表達(dá)呈顯著增高趨勢(shì)；與對(duì)照組比較，LTC14細(xì)胞接受相同濃度LPS刺激不同時(shí)間后JAK2、STAT3、NLRP3、caspase1、IL-1β蛋白表達(dá)呈顯著增高趨勢(shì)；與LPS組對(duì)比，OM和LPS共同處理組、AG490和LPS共同處理組JAK2、STAT3、NLRP3、caspase1及IL-1β的蛋白表達(dá)顯著降低。結(jié)論 LPS呈一定的時(shí)間-劑量關(guān)系激活LTC14細(xì)胞JAK2/STAT3信號(hào)通路及NLRP3炎性小體；OM可能通過(guò)抑制JAK2/STAT3信號(hào)通路起到抑制NLRP3炎性小體活化的作用。

Objective To study the effects of oxymatrine (OM) on the activation of NLRP3 in pancreatic stellate cells (PSCs) induced by lipopolysaccharide (LPS).Methods By setting different doses of LPS (0, 2.5, 5, 10, 20, 40 μg/mL) and setting the same dosage of LPS (10 μg/mL) to stimulate LTC14 cells at different time (0, 1, 3, 6, 9, 12 h), the dose-effect relationship of LPS-induced inflammatory corpuscles activation was investigated by Western blotting. After using OM and JAK2 inhibitor AG490 to intervene LPS-induced LTC14 cell lines, the expression of related molecules in JAK2/STAT3 signaling pathway and NLRP3 inflammatory corpuscles -related protein were detected by Western blotting.Results Compared with the control group, the expression of JAK2, STAT3, NLRP3, caspase 1 and IL-1β protein in LTC14 cells were increased significantly after LPS stimulation at different concentrations. Compared with the control group, the expression of JAK2, STAT3, NLRP3, caspase 1 and IL-1β protein in LTC14 cells were increased significantly after LPS stimulation at the same concentration for different time. The protein expressions of JAK2, STAT3, NLRP3, caspase 1 and IL-1β were significantly decreased in LPS-treated group. Conclusion LPS activates JAK2/STAT3 signaling pathway and NLRP3 inflammatory corpuscles in LTC14 cells in a time-dose relationship. OM may inhibit NLRP3 inflammatory body activation by inhibiting JAK2/STAT3 signaling pathway.

國(guó)家自然科學(xué)基金資助項(xiàng)目（81500489）；天津市自然科學(xué)基金聯(lián)合資助青年項(xiàng)目（15JCQNJC45600）；天津市西青醫(yī)院科研基金（XQYYLX201603）