Mechanism of Shengmai Injection on Anti-Sepsis and Protective Activities of Intestinal Mucosal Barrier in Mice
Chinese Journal of Integrative Medicine, ISSN: 1993-0402, Vol: 28, Issue: 9, Page: 817-822
2022
- 6Citations
- 2Captures
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Metrics Details
- Citations6
- Citation Indexes6
- CrossRef4
- Captures2
- Readers2
Article Description
Objective: To study the mechanism of Shengmai Injection (SMI, 生脉注射液) on anti-sepsis and protective activities of intestinal mucosal barrier. Methods: The contents of 11 active components of SMI including ginsenoside Rb1, Rb2, Rb3, Rd, Re, Rf, Rg1, Rg2, ophioposide D, schisandrol A and schisantherin A were determined using ultra-performance liquid chromatography. Fifty mice were randomly divided into the blank, the model, the low-, medium- and high-dose SMI groups (0.375, 0.75, 1.5 mL/kg, respectively) by random number table, 10 mice in each group. In SMI group, SMI was administrated to mice daily via tail vein injection for 3 consecutive days, while the mice in the blank and model groups were given 0.1 mL of normal saline. One hour after the last SMI administration, except the blank group, the mice in other groups were intraperitoneally injected with lipopolysaccharide (LPS) saline solution (2 mL/kg) at a dosage of 5 mL/kg for development of endotoxemia mice model. The mice in the blank group were given the same volume of normal saline. Inflammatory factors including interferon-γ (INF-γ), tumor necrosis factor-α (TNF-α), interleukin (IL)-2 and IL-10 were measured by flow cytometry. Myosin light-chain kinase (MLCK), nuclear factor κB (NF-κB) levels, and change of Occludin proteins in jejunum samples were analyzed by Western blot. Results: The decreasing trends of INF-γ, TNF-α and IL-2 were found in serum of SMI treatment groups. In SMI-treated mice, the content of Occludin increased and MLCK protein decreased compared with the model group (P<0.05 or P<0.01). The content of cellular and nuclear NF-κB did not change significantly (P>0.05). Conclusion: SMI may exert its anti-sepsis activity mainly through NF-κB-pro-inflammatory factor-MLCK-TJ cascade.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85109986993&origin=inward; http://dx.doi.org/10.1007/s11655-021-3292-y; http://www.ncbi.nlm.nih.gov/pubmed/34241804; https://link.springer.com/10.1007/s11655-021-3292-y; http://sciencechina.cn/gw.jsp?action=cited_outline.jsp&type=1&id=7264960&internal_id=7264960&from=elsevier; https://dx.doi.org/10.1007/s11655-021-3292-y; https://link.springer.com/article/10.1007/s11655-021-3292-y
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