Bibliographic Details
| Title: |
The role of dexmedetomidine in immune tissue and inflammatory diseases: a narrative review. |
| Authors: |
CHEN, R., DOU, X.-K., DAI, M.-S., SUN, Y., SUN, S.-J., WU, Y. |
| Source: |
European Review for Medical & Pharmacological Sciences; Nov2022, Vol. 26 Issue 21, p8030-8038, 9p |
| Abstract: |
OBJECTIVE: Adrenergic receptors belong to the G protein-coupled receptor family and are one of the important targets of modern drug therapy. Dexmedetomidine (DEX) is a highly selective agonist of alpha2 receptor, a member of the adrenergic receptor family, which are widely found in immune tissues and which mediate the biological behaviour of the inflammatory immune system. This review mainly summarizes the role of DEX in immune tissue and inflammation-related diseases, to provide a theoretical basis for clinical treatment. MATERIALS AND METHODS: We searched the PUBMED, EMBASE, and Cochrane libraries separately to obtain published literature on DEX related to immune tissue and inflammatory diseases. The mesh (dexmedetomidine, microglia, astrocytes, spleen, marrow, lymph nodes) and their corresponding keywords used for the searches, and no time limit for retrieval. The latest search was conducted on July 1, 2022. RESULTS: By reading a lot of relevant literature, we found that DEX reduces the inflammatory response of brain tissue by interfering with microglia and astrocytes. DEX can regulate the expression of CD40 and CD86 markers on the surface of splenocytes and reduce the secretion of inflammatory cytokines by splenocytes. In addition, we found that DEX reduced inflammation-related diseases such as neuroinflammation, myocarditis, liver cirrhosis, osteoarthritis, upper respiratory tract infection, pancreatitis, spinal tuberculosis, pulpitis, colon inflammation and rheumatoid arthritis, and improved prognosis. CONCLUSIONS: DEX has anti-inflammatory and improved prognosis in many inflammatory related diseases and is expected to become a targeted drug for the treatment of inflammatory diseases. [ABSTRACT FROM AUTHOR] |
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| Database: |
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