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灵芝中的高分子量多糖可减轻脂多糖诱导的肝损伤小鼠的炎症反应、肠道微生物群和肝脏代谢组学变化。

High molecular weight polysaccharides from Ganoderma lucidum attenuates inflammatory responses, gut microbiota, and liver metabolomic in lipopolysaccharide-induced liver injury mice.

作者信息

Guo Weiling, Liu Wenkun, Liang Peng, Ni Li, Lv Xucong, Fan Jinlin, Shi Feifei

机构信息

Institute of Food Science and Technology, College of Biological Science and Engineering, Fuzhou University, Fuzhou 350108, China.

Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou 350001, China.

出版信息

Int J Biol Macromol. 2025 Jan;287:138400. doi: 10.1016/j.ijbiomac.2024.138400. Epub 2024 Dec 8.

Abstract

High molecular weight polysaccharides (GLPH, ≥300 kDa) are the major compounds of Ganoderma lucidum with improving liver function. However, the effect of GLPH on improving acute liver injury (ALI) wasn't revealed. Herein, the ameliorating effects and mechanisms of GLPH were revealed in lipopolysaccharide (LPS)-ALI mice. The results indicated that GLPH intervention (100 mg/kg day) reduced the serum ALT (22.67 ± 6.48 U/L), AST (21.19 ± 7.08 U/L), ALP (56.98 ± 12.71 U/L), GGT (1.48 ± 0.22 U/L) levels in ALI mice (p < 0.01). GLPH activated the hepatic antioxidant enzymes activity [SOD (3.75 ± 1.17 U/mg prot.) and CAT (3.01 ± 0.85 U/mg prot.)] and suppressed the hepatic inflammatory cytokines production [TNF-α (40.14 ± 8.15 pg/mg prot.), IL-1β (35.47 ± 10.90 pg/mg prot.), and IL-6 (8.44 ± 1.71 pg/mg prot.)] by regulating the Nrf2/OH-1 and Tlr4/NF-κB pathway (p < 0.05). Furthermore, GLPH regulated the abundance of Bifidobacterium, Akkermansia, Anaerovorax, and Tyzzerella, which associated with cecal SCFAs, hepatic inflammatory cytokines and antioxidant enzymes. GLPH significantly changed 85 liver metabolites (p < 0.01), which is beneficial for prevent the development of ALI. These results suggested GLPH displayed promising prebiotic properties in relieving ALI, regulating gut microbiota and liver metabolism.

摘要

高分子量多糖(GLPH,≥300 kDa)是灵芝中具有改善肝功能作用的主要化合物。然而,GLPH对改善急性肝损伤(ALI)的作用尚未见报道。在此,我们揭示了GLPH在脂多糖(LPS)诱导的ALI小鼠中的改善作用及其机制。结果表明,GLPH干预(100 mg/kg/天)可降低ALI小鼠血清中的谷丙转氨酶(ALT,22.67±6.48 U/L)、谷草转氨酶(AST,21.19±7.08 U/L)、碱性磷酸酶(ALP,56.98±12.71 U/L)、γ-谷氨酰转肽酶(GGT,1.48±0.22 U/L)水平(p<0.01)。GLPH激活了肝脏抗氧化酶活性[SOD(3.75±1.17 U/mg蛋白)和CAT(3.01±0.85 U/mg蛋白)],并通过调节Nrf2/OH-1和Tlr4/NF-κB通路抑制了肝脏炎性细胞因子的产生[TNF-α(40.14±8.15 pg/mg蛋白)、IL-1β(35.47±10.90 pg/mg蛋白)和IL-6(8.44±1.71 pg/mg蛋白)](p<0.05)。此外,GLPH调节了双歧杆菌属、阿克曼氏菌属、厌氧食菌属和泰泽菌属的丰度,这些菌与盲肠短链脂肪酸、肝脏炎性细胞因子和抗氧化酶有关。GLPH显著改变了85种肝脏代谢物(p<0.01),这有利于预防ALI的发展。这些结果表明,GLPH在缓解ALI、调节肠道微生物群和肝脏代谢方面具有良好的益生元特性。

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