Potential role of β-carotene-modulated autophagy in puerperal breast inflammation (Review)

Abstract

Puerperal breast inflammation is common in the first 6-8 weeks postpartum, and without proper management, may lead to a decrease in breastmilk production and early cessation of breastfeeding. Recent studies showed that carotenoids decrease the severity of puerperal breast inflammation. This article summarizes the significant findings on β-carotene with a potential role as an autophagy modulator in puerperal breast inflammation. Puerperal milk stasis causes an increase in inflammatory cytokines and inflammatory cells, leading to reactive oxygen species (ROS) activation that causes oxidative damage to mammary glands and affects breast milk secretion. β-carotene has an anti-inflammatory effect related to its ROS-scavenging activity and modulates autophagy, thus stimulating the removal of damaged cellular structures and supporting milk gland survival. β-carotene modulates autophagy through phosphorylation of NF-κB, JNK, p38, Akt, and Nrf2, affects the ratio of Microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I, and has a role in the regulation of the JAK2/STAT3, PI2K/Akt/mTOR and AMPK pathways. Although the in vitro and in vivo studies showed promising results, further studies on humans are required to better conclude the potential role of β-carotene in managing puerperal breast inflammation.

Keywords: ROS; autophagy; breast milk; inflammation; puerperal; β-carotene.

Figure 1

Model of the inflammatory response within a lactating breast and the role of β-carotene as an antioxidant and autophagy modulator.

Figure 2

β-carotene scavenges excessive ROS and modulates autophagy through the phosphorylation of several proteins involved in autophagy, affecting JAK/STAT3, PI2K/Akt/mTOR, and the AMPK pathways, β-carotene also affects autophagosome formation and autophagic flux. ROS, reactive oxygen species.