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参苓白术散调控菌群代谢相关蛋白和TLR4/NF-κB/NLRP3炎症轴改善溃疡性结肠炎的机制研究
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篇名： 参苓白术散调控菌群代谢相关蛋白和TLR4/NF-κB/NLRP3炎症轴改善溃疡性结肠炎的机制研究
TITLE： Mechanism of Shenling baizhu san in ameliorating ulcerative colitis via regulating flora metabolism-related proteins and TLR4/NF-κB/NLRP3 inflammatory axis
摘要： 目的 研究参苓白术散（SLBZS）改善溃疡性结肠炎（UC）的作用机制。方法将小鼠随机分为正常组、模型组及SLBZS低、中、高剂量组（3、6、12g/kg），每组10只。除正常组外，其余各组小鼠自由饮用3%葡聚糖硫酸钠溶液7d，以诱导UC模型。在造模的同时，各组小鼠灌胃相应药液/双蒸水，每日1次，连续7d。末次给药后，观察小鼠结肠组织病理形态学变化，检测血清中炎症因子[肿瘤坏死因子α（TNF-α）、白细胞介素1β（IL-1β）、IL-18]水平，检测肝脏、胆囊、结肠组织中总胆汁酸含量，检测结肠组织中NOD样受体热蛋白结构域相关蛋白3（NLRP3）表达水平，检测肝脏/结肠组织中菌群代谢相关蛋白[G蛋白偶联受体41（GPR41）、GPR43、法尼醇X受体（FXR）、G蛋白偶联胆汁酸受体1（TGR5）、黄素单加氧酶3（FMO3）、细胞色素P450家族27亚家族A成员1（CYP27A1）、CYP7A1]和Toll样受体4（TLR4）/核因子κB（NF-κB）/NLRP3炎症轴相关蛋白[TLR4、NF-κB、磷酸化NF-κB（p-NF-κB）、髓样分化因子88（MyD88）、NLRP3、凋亡相关斑点样蛋白（ASC）、胱天蛋白酶1（caspase-1）]表达水平。结果与模型组相比，SLBZS中、高剂量组小鼠结肠组织损伤程度减轻，炎症细胞浸润减少；血清中TNF-α、IL-1β、IL-18水平，肝脏、结肠中总胆汁酸含量，肝脏组织中FMO3、CYP7A1和结肠组织中TLR4、p-NF-κB、NF-κB、MyD88、NLRP3、ASC、caspase-1的蛋白表达水平均显著降低（P＜0.05）；胆囊中总胆汁酸含量以及结肠组织中GPR41、GPR43和肝脏组织中CYP27A1、FXR、TGR5的蛋白表达水平均显著升高（P＜0.05）。结论SLBZS可能通过调控菌群代谢相关蛋白表达、抑制TLR4/NF-κB/NLRP3炎症轴异常激活，减轻结肠炎症损伤，从而改善UC病理状态。
ABSTRACT： Abstract OBJECTIVE To investigate the mechanism of Shenling baizhu san （SLBZS） in ameliorating ulcerative colitis （UC）. METHODS Mice were randomly divided into normal group， model group， and low-， medium-， high-dose SLBZS groups （3， 6， 12 g/kg）， with 10 mice in each group. Except for the normal group， mice in other groups were given free access to 3% dextran sulfate sodium solution for 7 days to establish UC models. Simultaneously， mice in each group were intragastrically administered corresponding medicinal liquid or double-distilled water once a day for consecutive 7 days. After the last administration， the histopathological morphology of colon tissues was observed； the serum levels of inflammatory factors including tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β） and IL-18 were detected； the total bile acid contents in liver， gallbladder and colon tissues were determined； the expression level of NOD-like receptor family pyrin domain-containing protein 3 （NLRP3） in colon tissues was tested. The expression levels of flora metabolism-related proteins [G protein-coupled receptor 41（GPR41），GPR43，farnesoid X receptor （FXR）， G protein-coupled bile acid receptor 1 （TGR5）， flavin-containing monooxygenase 3 （FMO3）， cytochrome P450 family 27 subfamily A member 1 （CYP27A1）， CYP7A1] in liver or colon tissues， as well as the proteins related to Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB）/NLRP3 inflammatory axis [TLR4， NF-κB， phosphorylated NF-κB （p-NF-κB）， myeloid differentiation factor 88 （MyD88）， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， caspase-1] in colon tissues were measured. RESULTS Compared with the model group， the colon tissue injury and inflammatory cell infiltration were alleviated in medium- and high-dose SLBZS groups. The serum levels of TNF-α， IL-1β and IL-18， total bile acid contents in liver and colon tissues， as well as the protein expression levels of FMO3 and CYP7A1 in liver tissues， TLR4， p-NF-κB， NF-κB， MyD88， NLRP3， ASC and caspase-1 in colon tissues were significantly decreased （P＜0.05）. Meanwhile， the total bile acid content in gallbladder， the protein expression levels of GPR41 and GPR43 in colon tissues， along with CYP27A1， FXR and TGR5 in liver tissues were significantly increased （P＜0.05）. CONCLUSIONS SLBZS may relieve colonic inflammatory injury and ameliorate UC by regulating the expression of flora metabolism-related proteins and inhibiting the abnormal activation of TLR4/NF-κB/NLRP3 inflammatory axis.
期刊： 2026年第37卷第15期
作者： 徐佳佳；游宇；王佼曼；刘玉晖；常诗瑶；贺智贤；李萍；王紫嫣；熊魏；韩飞
AUTHORS： XU Jiajia，YOU Yu， WANG Jiaoman，LIU Yuhui，CHANG Shiyao，HE Zhixian，LI Ping，WANG Ziyan，XIONG Wei，HAN Fei
关键字： 参苓白术散；溃疡性结肠炎；TLR4/NF-κB/NLRP3炎症轴；肠道菌群；胆汁酸代谢
KEYWORDS： Shenling baizhu san； ulcerative colitis； TLR4/NF-κB/NLRP3 inflammatory axis； intestinal flora； bile acid metabolism
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