Antifertility effect
Luteolin has significant dose-dependent anti-implantation activity and can interfere with the implantation process of fertilized eggs in the endometrium. Its mechanism of action may involve the regulation of the physiological environment of the endometrium, such as inhibiting the expression of cytokines or adhesion molecules required for embryo implantation by changing the thickness of the endometrium, epithelial cell morphology or secretory function.
Estrogen-like effect
When used alone, luteolin exhibits estrogen-like activity, which can promote uterine weight increase, diameter expansion, endometrial thickening and epithelial cell height increase. This effect may be achieved by activating estrogen receptors (ER), especially ERα or ERβ subtypes, thereby inducing the expression of genes related to uterine tissue proliferation.
Anti-estrogen effect
When luteolin is used in combination with synthetic estrogens such as ethinyl estradiol, its effect turns to anti-estrogen. Possible mechanisms include: competitive inhibition of estrogen binding to receptors, or accelerating estrogen metabolism and clearance by regulating the activity of estrogen metabolizing enzymes (such as CYP450). In addition, luteolin may downregulate estrogen receptor expression or block estrogen signal transduction pathways, thereby weakening the biological effects of exogenous estrogen.
Clinical significance
The bidirectional hormone regulation of luteolin makes it potentially useful in the field of reproductive health. For example, in scenarios where anti-fertility is required, its anti-implantation activity can provide a non-hormonal contraceptive option; in hormone replacement therapy, combined use with synthetic estrogen may reduce dose-dependent side effects. However, it should be noted that its intensity and safety still need to be verified by further clinical trials, especially the long-term effects on the endometrium and interactions with other drugs.