Abstract
Myrrh is the oleo-gum resin of mainly Commiphora molmol and as a powdered substance, one compound in the traditional medicinal product Myrrhinil-Intest®,
which has been used for the treatment of unspecific, inflammatory intestinal disorders.
The aim of the present study was to evaluate the antispasmodic effect of myrrh under
healthy and inflamed conditions, and to evaluate a calcium-antagonistic effect as
a possible mode of action. Therefore, an ethanolic myrrh extract was tested for its
effects on muscle tone and acetylcholine-induced contractions in untreated and inflamed
rat ileum/jejunum preparations. Inflammation was experimentally induced by 2,4,6-trinitrobenzene
sulfonic acid (10 mM, 30 min). Additionally, the effect of the calcium channel agonist
Bay K8644 in the presence of varying myrrh extract concentrations was examined. Myrrh
extract (0.99 mg/mL) suppressed the acetylcholine-induced contraction down to 25.8 %
in untreated and 15.2 % in inflamed preparations. Myrrh extract (0.15; 0.25 and 0.35 mg/mL)
induced a concentration-dependent rightward shift of the Bay K8644 concentration-response
curve in untreated and inflamed preparations with a significant EC50 shift. Schild analysis resulted in a pA2 value of 0.93 for untreated preparations.
Increasing myrrh extract concentrations induced a concentration-dependent decrease
of the agonistic maximum effect in untreated and inflamed preparations down to 15.8 %
and 25.8 %, respectively, for the highest concentration leading to a pD2 value of
0.58. Myrrh extract reduced intestinal muscle tone and acetylcholine-induced contraction
of untreated and inflamed ileum/jejunum preparations based on dual calcium antagonism
characterized by a right shift of the agonistic dose-response curve and a depression
of the maximum effect. The resulting reduction of intestinal motility and spasmolytic
effects provide a rationale for the symptom treatment of intestinal disorders such
as irritable bowel syndrome.
Key words
Commiphora molmol
- Burseraceae - myrrh - calcium antagonist - gastrointestinal tract - inflammation
