Lentinan Prevents Lipopolysaccharide-Induced Preterm Birth and Improves Offspring Survival Rate in Mice

Pingping Dong, Xiaoyan Liang, Feng Wang, Guoqing Gu, Fengyun Su, Haimin Wang

Article ID: 7986
Vol 38, Issue 4, 2024
DOI: https://doi.org/10.23812/j.biol.regul.homeost.agents.20243804.254
Received: 20 April 2024; Accepted: 20 April 2024; Available online: 20 April 2024; Issue release: 20 April 2024

Abstract

Background: Preterm birth is a major cause of neonatal mortality and morbidity, with inflammation being a crucial contributor to its occurrence. The nuclear factor-kappa B (NF-κB) pathway serves as an important regulator of inflammatory responses and is strongly associated with preterm birth. However, lentinan has been recognized for its immunomodulatory and anti-inflammatory effects. Therefore, this study aimed to delve into the potential impact as well as the underlying mechanism of lentinan on preterm birth. Methods: In this study, we used a lipopolysaccharide (LPS)-induced preterm birth model in mice to evaluate the effect of lentinan on preterm birth and its influence on the NF-κB inflammatory pathway. Mice were randomly assigned to the control, LPS, and LPS+Lentinan intervention groups. The levels of inflammatory factors and expression of NF-κB pathway-related proteins in uterine tissues were assessed using enzyme-linked immunosorbent assay (ELISA), western blot analysis, and immunohistochemistry techniques. Results: Compared to the LPS group, the LPS+Lentinan intervention group showed a significant reduction in the rate of preterm birth (p < 0.01), as well as improvements in offspring survival and birth weight (p < 0.01). Moreover, lentinan inhibited the expression of inflammation-related proteins (such as jun proto-oncogene (C-JUN) and phosphorylated(p)-P65) in LPS-induced uterine smooth muscle (p < 0.01), while reducing the upregulation of inflammatory factors (such as tumor necrosis factor (TNF)-α, interleukin (IL)-6; p < 0.01). These results suggest that lentinan may exert anti-inflammatory effects by inhibiting the activation of the NF-κB pathway. Conclusion: Lentinan effectively prevents LPS-induced preterm birth in mice and improves offspring survival. Its mechanism may be related to the inhibition of the activation of NF-κB inflammatory pathway in uterine smooth muscle. This finding provides a potential natural drug candidate for the development of new interventions to prevent preterm birth, thereby reducing neonatal mortality and associated complications.


Keywords

lentinan polysaccharides;NF-κB inflammatory pathway;preterm birth prevention;lipopolysaccharide-induced;neonatal survival rate


References

Supporting Agencies



Copyright (c) 2024 Pingping Dong, Xiaoyan Liang, Feng Wang, Guoqing Gu, Fengyun Su, Haimin Wang




This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).