Dysmenorrhea refers to a kind of uterine cramping
pain that occurs in women during the period of menstrual.
Guizhi Fuling Capsules are mainly used for the treatment of various
pain syndromes and especially effective in treating primary
dysmenorrhea. However, the research on its modern pharmacology and mechanism of action have not been thoroughly carried out. It is not clear about the main active ingredients, potential targets and metabolic pathways involved in its efficacy. Therefore, this research project employed
estradiol benzoate sensitization combined with
oxytocin pain to construct the cold coagulation syndrome
dysmenorrhea model, observed the anti-
dysmenorrhea effect of
Guizhi Fuling Capsules, and used the metabolomics to explore its mechanism. The results showed that
Guizhi Fuling Capsules could considerably reduce the number of writhing times in
dysmenorrhea rats, increasing the level of
PGE2 and β-EP and reducing the contents of PGF2α in rat serum. Pathological sections of uterus and ovaries also showed that
Guizhi Fuling Capsules could significantly relieve
endometrial hyperplasia and improve ovarian function. The LC/MS-based metabolomics of rat uterine indicated that the model group has a great deviation from the control group. Compared with the model group, the
Guizhi Fuling Capsules group had a tendency to shift to the control group, and the main metabolic changes was mainly concentrated on saturated and
unsaturated fatty acids. Among them,
arachidonic acid is in a pivotal position, and the expression of its rate-limiting
enzyme (COX-2) involved in its
cyclooxygenase metabolic pathway was significantly up-regulated in the model group, but significantly decreased after the intervention of
Guizhi Fuling Capsules. In conclusion,
Guizhi Fuling Capsules can effectively relieve primary
dysmenorrhea, and this effect may be attributed to the regulation effects of
Guizhi Fuling Capsules on endogenous metabolism, such as inhibiting
arachidonic acid converted to
prostaglandins through downregulate the expression of COX-2, which plays an anti-inflammatory effect.