Chen Yu-Sheng, Chen Quan-Zhan, Wang Zhen-Jiong, Hua Chun
School of Food Science, Nanjing Xiaozhuang University, Nanjing, China,
School of Food Science, Nanjing Xiaozhuang University, Nanjing, China.
Pharmacology. 2019;103(3-4):143-150. doi: 10.1159/000493896. Epub 2019 Jan 23.
Ganoderma lucidum Polysaccharides (GLPS) were found to possess various pharmacological properties including anti-inflammatory and hepatoprotective activities. However, the effect and possible mechanism of GLPS treatment on liver injury have not yet been reported. Therefore, this study aimed to explore the potential anti-inflammatory and hepatoprotective effects and possible mechanism of GLPS in carbon tetrachloride (CCl4)-induced acute liver injury mice.
GLPS significantly reduced the activation of NLRP3 inflammasome and improved liver function in liver injury mice. It significantly inhibited CCl4-induced changes of alanine aminotransferase and aspartate aminotransferase activities in serum, as well as nitric oxide synthase (NOS) and cytochrome P450 2E1 (CYP2E1) activities in liver tissue; it also remarkably decreased levels of liver weight and index, total bilirubin, interleukin (IL)-1β, IL-18, IL-6 and tumor necrosis factor-α in serum, as well as malondialdehyde and IL-1β in liver tissue. Protein expression levels of liver NLRP3, ASC, and Caspase-1 were also downregulated, while the glutathione level in liver tissue was remarkably enhanced in GLPS groups compared to that of the model group. Key Message: These results suggested that GLPS may be a potential for the prevention and treatment of acute liver injury with liver inflammation. The possible mechanism may be related to the inhibition of free radical lipid peroxidation, NOS, and CYP2E1 activities and activation of liver inflammatory factors.
灵芝多糖(GLPS)具有多种药理特性,包括抗炎和保肝活性。然而,GLPS治疗肝损伤的效果及可能机制尚未见报道。因此,本研究旨在探讨GLPS对四氯化碳(CCl4)诱导的急性肝损伤小鼠的潜在抗炎和保肝作用及可能机制。
GLPS显著降低肝损伤小鼠中NLRP3炎性小体的激活并改善肝功能。它显著抑制CCl4诱导的血清中谷丙转氨酶和谷草转氨酶活性的变化,以及肝组织中一氧化氮合酶(NOS)和细胞色素P450 2E1(CYP2E1)的活性;还显著降低血清中肝重和肝指数、总胆红素、白细胞介素(IL)-1β、IL-18、IL-6和肿瘤坏死因子-α的水平,以及肝组织中丙二醛和IL-1β的水平。与模型组相比,GLPS组肝组织中NLRP3、ASC和半胱天冬酶-1的蛋白表达水平也下调,而肝组织中谷胱甘肽水平显著升高。关键信息:这些结果表明,GLPS可能具有预防和治疗伴有肝脏炎症的急性肝损伤的潜力。其可能机制可能与抑制自由基脂质过氧化、NOS和CYP2E1活性以及激活肝脏炎症因子有关。