Pharmacodynamics assessment of β-carboline from the roots of Psammosilene tunicoides as analgesic compound

Ethnopharmacological relevance: The root of Psammosilene tunicoides (W. C. Wu et C. Y. Wu) is a well-known medicinal herb for the treatment of pain, hemostasia and rheumatoid arthritis among Chinese people. Aim of the study: The present study aimed to investigate the antinociceptive activity and mechanism of beta-carboline alkaloids 1-4 which were extracted from the roots of P. tunicoides. Materials and methods: The analgesic effects were evaluated using peripheral and central pain mouse models of nociception, including the formalin test and the tail flick test. The levels of glutamic acid (Glu) and nitric oxide (NO) in cerebellar cortexes and spinal cords (L4-6) were determined. The anti-inflammatory of all compounds were then assessed on RAW264.7 cells. Results: Our results showed that compounds 1-4 had significant analgesic effects on both phases of formalin test of mice. Furthermore, all compounds showed suppressive effects on Glu in the brain and NO levels in the brain cortex and the spinal cord. Except for compound 1, the others could extend the pain threshold of hot water tail-flick in mice. In addition, compounds 2 and 3 (60 mu mol/kg) could decrease GABAA alpha 1 protein levels in spinal cord. All compounds exhibited anti-inflammatory effects by inhibiting lipopolysaccharide (LPS)-induced NO production in RAW264.7 cells with half-maximal inhibitory concentration (IC50) 1.1-34.9 mu M. Conclusion: beta-carboline alkaloids from the roots of P. tunicoides had significant analgesic activity by both central and peripheral mechanisms. Our findings suggested that regulating the release of NO or Glu or GABA alpha 1 are some of the mechanisms of analgesic activity of beta-carboline alkaloids.

Automated summary

Beta-carboline alkaloids from the roots of P. tunicoides have significant analgesic activity by both central and peripheral mechanisms, which may be mediated by regulating the release of NO, Glu, or GABA alpha 1.