Effects and mechanism of puerarin on lactation of postpartum hypogalactia mice

TL;DR

Puerarin improves milk production in mice with low postpartum lactation by boosting hormone levels and activating key signaling pathways.

Contribution

Puerarin's mechanism in promoting lactation via PRLR/JAK2/STAT5 pathway activation is newly identified in postpartum hypogalactia mice.

Findings

Puerarin significantly improved lactation yield and mammary gland development in hypogalactia mice.

Puerarin increased β-casein, FAS, and GLUT1 expression levels in the mice.

Puerarin stimulated PRL, E2, and P4 secretion and upregulated PRLR, JAK2, and STAT5a expression.

Abstract

Insufficient breast milk supply is a common reason cited for discontinuing breastfeeding prematurely. Natural galactagogues offer promise as a solution for mothers with low milk production. This study aimed to explore puerarin’s potential effects and underlying mechanism on lactation of postpartum hypogalactia mice.

Postpartum mice were randomly assigned to five groups: control group, agalactosis model group, domperidone group (3.5 mg/kg), low dose puerarin group (18 mg/kg), and high dose puerarin group (72 mg/kg). The effects of puerarin on postpartum hypogalactia mice were evaluated by lactation indicators and pathological morphology. Related hormones and prolactin receptor (PRLR)/Janus kinase 2 (JAK2)/signal transduction and activator (STAT) 5 signaling pathway were also measured.

Puerarin significantly improved lactation yield and stimulated mammary gland development in postpartum hypogalactia mice. Additionally, puerarin increased the expression levels of β-casein, fatty acid synthase (FAS), and glucose transporter 1 (GLUT1). Mechanically, puerarin stimulated secretion of prolactin (PRL), estradiol (E2), and progesterone (P4) in agalactosis mice. Puerarin also substantially increased PRLR, JAK2, and STAT5a expression levels in postpartum hypogalactia mice.

This study suggested that puerarin may promote lactation by stimulating PRL secretion and activating the PRLR/JAK2/STAT5 signaling pathway.

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