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Quercetin Prevents Lipopolysaccharide-Induced Experimental Preterm Labor in Mice and Increases Offspring Survival
Xinxiu Lin1, Qiaozhen Peng1, Jiejie Zhang1
1Department of Obstetrics and Gynecology, Xiangya Hospital Central South University, No.87 Xiangya Road, Changsha, 410008, China.
Premature labor is still a worldwide problem, causing serious social economic burden and family burden. Currently, there is no effective way to prevent preterm labor. Since inflammation increases the risk of preterm birth and quercetin is reported to have anti-inflammation, immune-enhancement, and antioxidative effects, this study aims to explore whether quercetin exerts inhibitory effect on preterm labor in mice and increases offspring survival. Lipopolysaccharide (LPS) is one of the commonly used drugs in the inflammatory animal model of preterm birth. On day 15 of pregnancy, mice received a dose of vehicle phosphate-buffered saline (PBS) or a dose of quercetin (low concentration, 30 mg/kg; medium concentration, 90 mg/kg; high concentrations, 150 mg/kg) via oral gavage. After 2 h, mice received a dose of LPS (50 μg/kg) or vehicle intraperitoneally (i.p.). In the absence of quercetin, a 100% incidence of preterm labor was observed in LPS-treated mice, and the fetuses were all died. Medium concentration of quercetin significantly prevented 63.5% of LPS-induced inflammatory preterm labor, and the survival rate of pups on day 22 was 83.76%. Specifically, quercetin significantly inhibited LPS-induced upregulation of NF-kappa-B/P65(RELA), AP-1/C-JUN(JUN), cyclooxygenase-2(PTGS2), and interleukin 6(IL6) in mice myometrium on mRNA level and inhibited the upregulation of P65 and C-JUN on protein level. Based on these observations, we concluded that quercetin exerts inhibitory effect on LPS-induced experimental mice preterm labor and increases offspring survival through a mechanism involving NF-κB/AP-1 pathway.
Premature labor is still a worldwide problem, causing serious social economic burden and family burden. Currently, there is no effective way to prevent preterm labor. Since inflammation increases the risk of preterm birth and quercetin is reported to have anti-inflammation, immune-enhancement, and antioxidative effects, this study aims to explore whether quercetin exerts inhibitory effect on preterm labor in mice and increases offspring survival. Lipopolysaccharide (LPS) is one of the commonly used drugs in the inflammatory animal model of preterm birth. On day 15 of pregnancy, mice received a dose of vehicle phosphate-buffered saline (PBS) or a dose of quercetin (low concentration, 30 mg/kg; medium concentration, 90 mg/kg; high concentrations, 150 mg/kg) via oral gavage. After 2 h, mice received a dose of LPS (50 μg/kg) or vehicle intraperitoneally (i.p.). In the absence of quercetin, a 100% incidence of preterm labor was observed in LPS-treated mice, and the fetuses were all died. Medium concentration of quercetin significantly prevented 63.5% of LPS-induced inflammatory preterm labor, and the survival rate of pups on day 22 was 83.76%. Specifically, quercetin significantly inhibited LPS-induced upregulation of NF-kappa-B/P65(RELA), AP-1/C-JUN(JUN), cyclooxygenase-2(PTGS2), and interleukin 6(IL6) in mice myometrium on mRNA level and inhibited the upregulation of P65 and C-JUN on protein level. Based on these observations, we concluded that quercetin exerts inhibitory effect on LPS-induced experimental mice preterm labor and increases offspring survival through a mechanism involving NF-κB/AP-1 pathway.
