Abstract

AbstractSodium Danshensu (SDSS), a vital constituent of Salvia miltiorrhiza Bunge, reportedly protects the myocardium and inhibits platelet aggregation, while displaying antiatherosclerotic, hypolipidemic, and anti‐inflammatory properties. In the research, the immune regulatory influences and mechanisms of SDSS on the T lymphocytes in the human peripheral blood were investigated. The results showed that administering specific SDSS doses enhanced T lymphocyte growth, while distinctly promoting their tumor cell cytotoxicity. However, SDSS showed no effect on the proliferation of A549, HCT116, and K562 cancer cells. The gene expression of the IFN‐γ, IL‐4, IL‐2, and IL‐6 cytokines secreted by T cells was positively regulated. Furthermore, SDSS dose‐dependently facilitated phosphorylated extracellular regulated protein kinase (p‐ERK) as well as phosphorylated c‐Jun N‐terminal kinase (p‐JNK) protein expression, increased IKKβ and Ikappa B kinase α (IKKα) protein expression and decreased the nuclear factor kappa‐B kinase α (IκBα) inhibitor; negatively regulated p‐p65 protein expression in the cytoplasm, and positively in the nucleus. In addition, blockage of protein expression with specific ERK, JNK, or IκBα inhibitors significantly restricted the T lymphocyte growth induced by SDSS, identifying the specific regulatory influence of SDSS on T lymphocytes via the signaling pathways involving nuclear factor kappa‐B (NF‐κB) and mitogen‐activated protein kinase (MAPK). In conclusion, SDSS can explicitly encourage T lymphocyte propagation in the peripheral blood of humans, while enhancing their cytotoxicity by activating the pathways involving NF‐κB and MAPK.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.