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Post‐treatment with yiqifumai injection and its main ingredients attenuates lipopolysaccharide‐induced microvascular disturbance in mesentery and ileum
Author(s) -
Ayididaer Ayan,
Sun Kai,
Pan ChunShui,
Yan Li,
Liu YuYing,
Li DanTong,
Fan JingYu,
Han JingYan
Publication year - 2021
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12680
Subject(s) - lipopolysaccharide , downregulation and upregulation , ileum , pharmacology , chemistry , umbilical vein , stimulation , edema , medicine , biochemistry , in vitro , gene
Objective To investigate the effect of Yiqifumai injection (YQFM), a compound Chinese medicine, and its main active ingredients on lipopolysaccharide (LPS)‐induced microvascular disturbance in mesentery and ileum. Methods Rats were infused with LPS (5 mg/kg/h) for 90 min. Thirty minutes after initiation of LPS administration, YQFM (160 mg/kg/h), Rb1 (5 mg/kg/h), Sch (2.5 mg/kg/h), or Rb1+Sch (5 mg/kg/h + 2.5 mg/kg/h) was infused until 90 min. Human umbilical vein endothelial cells (HUVECs) were incubated with LPS (100 ng/ml) for 90 min. YQFM (1 mg/ml), Rb1 (100 µM), Sch (100 µM), or Rb1+Sch (200 µM) was added 30 min after initiation of LPS stimulation. Results Yiqifumai injection and Rb1+Sch inhibited mesenteric venule hyperpermeability, suppressed microvillar erosion and submucosal edema, and protected claudin‐5 from downregulation and interleukin‐1β from upregulation in ileal tissues after LPS. Study in HUVECs confirmed the effect of YQFM and Rb1+Sch on JAM‐1 after LPS and revealed a similar effect on other junction proteins. Moreover, YQFM and Rb1+Sch attenuated the dysfunctional energy metabolism and the activation of TLR‐4/Src/NF‐κB signaling with Rb1 and Sch being partially effective. Conclusion These results demonstrated the beneficial effect of post‐treatment with YQFM, which is attributable to its main ingredient Rb1 and Sch, and likely mediated by targeting TLR‐4/Src/NF‐κB signaling pathway.