Li Chong, Lai Shu, Yi Ruokun, Zhou Xianrong, Zhao Xin, Li Qiang
Collaborative Innovation Center for Child Nutrition and Health Development, Chongqing Engineering Research Center of Functional Food, Chongqing Engineering Laboratory for Research and Development of Functional Food, Chongqing University of Education, Chongqing, People's Republic of China.
Department of Food and Nutrition, College of Medical and Life Science, Silla University, Busan, Republic of Korea.
J Inflamm Res. 2022 Aug 8;15:4499-4513. doi: 10.2147/JIR.S369176. eCollection 2022.
The liver protection of blood coral polysaccharide (BCP) was investigated.
We evaluated the effect of BCP on liver pathology, liver function, oxidation and inflammation-related indicators of D-Gal/LPS-induced acute liver failure (ALF) mice in vivo.
Liver index and liver pathology observation in mice showed that BCP could inhibit liver tissue swelling and hemorrhage, hepatocyte damage, and inflammatory infiltration in ALF. Serum liver function results showed that BCP effectively inhibits the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), total bilirubin (TBil), alkaline phosphatase (AKP), myeloperoxidase (MPO). High dose-blood coral polysaccharide (H-BCP) was better than silymarin. Serum antioxidant and immune results showed that BCP increased the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-Px), and inhibited the levels of malondialdehyde (MDA) and nitric oxide (NO). Also, BCP increased immunoglobulins G (IgG) and A (IgA) levels, thereby enhancing humoral immunity. Liver anti-inflammatory ELISA results showed that BCP reduced the levels of interleukin (IL)-6, IL-1β, IL-17, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, and enhanced the level of anti-inflammatory factor IL-10. H-BCP was the most effective treatment. Real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) of liver tissues confirmed that BCP increases the relative expression levels of antioxidant and anti-inflammatory-related cuprozinc superoxide dismutase (Cu/Zn-SOD, SOD1), manganese superoxide dismutase (Mn-SOD, SOD2), CAT, GSH, GSH-Px, and IL-10. In contrast, it inhibits inflammation-related genes IL-6, IL-1β, IL-17, TNF-α, IFN-γ, inducible nitric oxide synthase (iNOS, NOS2), and cyclooxygenase (COX)-2. In addition, BCP also inhibits the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and enhance B-cell inhibitor-α (IκB-α) gene relative expression in the liver, which may be related to NF-κB pathway inhibition.
BCP prevents D-Gal/LPS-induced ALF in mice, and its effect is concentration dependent.
研究血珊瑚多糖（BCP）的肝脏保护作用。
我们在体内评估了BCP对D-半乳糖/脂多糖（LPS）诱导的急性肝衰竭（ALF）小鼠的肝脏病理、肝功能、氧化和炎症相关指标的影响。
小鼠肝脏指数和肝脏病理观察表明，BCP可抑制ALF中肝组织肿胀、出血、肝细胞损伤和炎症浸润。血清肝功能结果显示，BCP有效抑制天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、乳酸脱氢酶（LDH）、总胆红素（TBil）、碱性磷酸酶（AKP）、髓过氧化物酶（MPO）水平。高剂量血珊瑚多糖（H-BCP）效果优于水飞蓟宾。血清抗氧化和免疫结果显示，BCP提高超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）和谷胱甘肽过氧化物酶（GSH-Px）水平，并抑制丙二醛（MDA）和一氧化氮（NO）水平。此外，BCP提高免疫球蛋白G（IgG）和A（IgA）水平，从而增强体液免疫。肝脏抗炎ELISA结果显示，BCP降低白细胞介素（IL）-6、IL-1β、IL-17、肿瘤坏死因子（TNF）-α和干扰素（IFN）-γ水平，并提高抗炎因子IL-10水平。H-BCP治疗效果最为显著。肝脏组织实时定量逆转录-聚合酶链反应（RT-qPCR）证实，BCP提高抗氧化和抗炎相关的铜锌超氧化物歧化酶（Cu/Zn-SOD，SOD1）、锰超氧化物歧化酶（Mn-SOD，SOD2）、CAT、GSH、GSH-Px和IL-10的相对表达水平。相反，它抑制炎症相关基因IL-6、IL-1β、IL-17、TNF-α、IFN-γ、诱导型一氧化氮合酶（iNOS，NOS2）和环氧化酶（COX）-2。此外，BCP还抑制肝脏中活化B细胞核因子κ轻链增强子（NF-κB）并提高B细胞抑制剂α（IκB-α）基因相对表达，这可能与NF-κB通路抑制有关。
BCP可预防D-半乳糖/LPS诱导的小鼠ALF，其作用呈浓度依赖性。
