Scholar - SciOpen

To investigate the protective effect and mechanism of docosahexaenoic acid-enriched phospholipids (DHA-PL) and eicosapentaenoic acid-enriched phospholipids (EPA-PL) on lipopolysaccharide (LPS)-induced acute liver injury.

Methods

DHA-PL and DHA-PL were obtained from the eggs of Sthenoteuthis oualaniensis and the body wall of Cucumaria frondosa, respectively. C57BL/6 male mice were randomly divided into four groups, i.e. control group, LPS-induced model group, LPS + DHA-PL group and LPS + EPA-PL group. The mice in the LPS + DHA-PL and LPS + EPA-PL groups were given DHA-PL and EPA-PL via the intragastric route at 400 mg/kg m_b on a daily basis for 28 days, respectively, while those in the control and model groups were gavaged with normal saline. The mice in the control group were injected with normal saline intraperitoneally at day 29, while those in the other groups were injected with LPS (10 mg/kg m_b) at an injection volume of 10 mL/kg m_b to establish a model of acute liver injury. The pathological changes of liver tissues were observed by hematoxylin-eosin (HE) staining. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured. The transcriptional levels and contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in liver tissues were detected by real-time quantitative polymerase chain reaction (PCR) and enzyme linked immunosorbent assay (ELISA), respectively. The phosphorylation levels of mitogen-activated protein kinases (MAPKs) such as extracellular regulated protein kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and nuclear factor (NF)-κB p65 were determined by Western blotting.

Results

DHA-PL and EPA-PL intervention effectively alleviated LPS-induced acute liver injury and reduced hepatic index and serum ALT and AST activities, decreased the hepatic mRNA expression and contents of TNF-α, IL-1β and IL-6, and down-regulated the phosphorylation of ERK1/2, JNK, p38 and NF-κB p65.

Conclusion

DHA-PL and EPA-PL can prevent LPS-induced acute liver injury in mice, and the mechanism may depend on regulation of the MAPKs and NF-κB signaling pathways.

Open Access Research Article Issue

Krill oil attenuates obesity-induced skeletal muscle atrophy in mice

Mengqing Zhou, Yuhong Yang, Yan Zheng, Zijian Wu, Chen Chen, Qijian Liang, Yu Yang, Hao Wu, Xin Guo, Lei Du

Food Science and Human Wellness 2025, 14(1): 9250018

Published: 14 February 2025

Abstract

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Obesity is associated with skeletal muscle mass loss and physical dysfunction. Krill oil (KO) has been shown to be beneficial in human health. However, the effect of KO on obesity-induced skeletal muscle atrophy is still unclear. In this study, the male C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity, and then were intragastric administration with 400 mg/kg bw KO for an additional 6 weeks. The results showed that KO treatment reduced body weight, fat accumulation and serum pro-inflammatory cytokines in HFD-induced obese mice. Importantly, KO treatment attenuated skeletal muscle atrophy in HFD-fed mice, as evidenced by preserving skeletal muscle mass, average myofiber cross-sectional area and grip strength. KO administration also mitigated obesity-induced ectopic lipid deposition and inflammatory response in skeletal muscle. Additionally, KO treatment inhibited the transcriptional activities of nuclear factor-κB (NF-κB ) p65 and forkhead box O 3a (FoxO3a), and then down-regulated muscle atrophy F-box (MAFbx) and muscle-specific RING finger protein 1 (MuRF1) protein levels in skeletal muscle from HFD-fed mice. KO administration also improved obesity-induced impaired muscle protein synthesis via activating PI3K/Akt pathway. Furthermore, KO treatment enhanced muscle mitochondrial biogenesis in HFD-induced obese mice via activating PGC-1α pathway. Collectively, KO might be developed as a potential nutritional supplement for the prevention and treatment of obesity-induced skeletal muscle atrophy.

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