Su Yue, Huang Jialu, Shi Panpan, Li Pingping, Huang Peng, Zeng Jianguo
College of Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi, China.
Hunan Key Laboratory of Traditional Chinese Veterinary Medicine, Hunan Agricultural University, Changsha, Hunan, China.
J Med Food. 2024 May;27(5):428-436. doi: 10.1089/jmf.2023.K.0242. Epub 2024 Mar 22.
Inflammatory bowel disease, a disease featured by intestinal epithelial barrier destruction and dysfunction, has been a constant threat to animal health. The primary objective of this research was to assess the impact of the extract derived from lotus leaves (LLE) on lipopolysaccharide (LPS) induced damage to the intestines in mice, as well as to investigate the fundamental mechanism involved. The LLE was prepared using ultrasonic extraction in this experiment, and the LLE total flavonoid content was 117.02 ± 10.73 mg/g. The LLE had strong antioxidant activity , as assessed by 2, 2-diphenyl-1-picrylhydrazyl, ferric reducing antioxidant power, and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) methods. In the experiment, different doses of LLE (50, 100, and 200 mg/kg) were administered for 2 weeks before LPS treatment in mice. The results revealed that LLE alleviates intestinal tissue damage in LPS-induced mice. In the jejunum tissue, LLE significantly upregulated mRNA and protein expression levels of tight junction proteins, such as ZO-1, , and , and decreased the contents of the inflammatory cytokines, interleukin (IL)-1, IL-6, and tumor necrosis factor-. Furthermore, the malondialdehyde and lactate dehydrogenase contents increased by LPS in the liver were significantly reduced after administration of LLE, and the total antioxidant capacity, superoxide dismutase, and reduced glutathione decreased by LPS were remarkably increased by LLE. It was found that LLE could relieve LPS-induced oxidative stress by upregulating mRNA and protein expression of and in jejunum tissue. In conclusion, LLE alleviates LPS-induced intestinal damage through regulation of the signal pathway to alleviate oxidative stress, reducing inflammatory factors and increasing the expression of tight junction proteins in mice.
炎症性肠病是一种以肠道上皮屏障破坏和功能障碍为特征的疾病,一直对动物健康构成威胁。本研究的主要目的是评估荷叶提取物(LLE)对脂多糖(LPS)诱导的小鼠肠道损伤的影响,并探究其 underlying 机制。本实验采用超声提取法制备LLE,其总黄酮含量为117.02±10.73mg/g。通过2,2-二苯基-1-苦基肼、铁还原抗氧化能力和2,2'-联氮-双-(3-乙基苯并噻唑啉-6-磺酸)法评估,LLE具有较强的抗氧化活性。在实验中,在对小鼠进行LPS处理前2周给予不同剂量的LLE(50、100和200mg/kg)。结果显示,LLE减轻了LPS诱导的小鼠肠道组织损伤。在空肠组织中,LLE显著上调紧密连接蛋白如ZO-1等的mRNA和蛋白表达水平,并降低炎症细胞因子白细胞介素(IL)-1、IL-6和肿瘤坏死因子-的含量。此外,给予LLE后,LPS诱导的肝脏中丙二醛和乳酸脱氢酶含量显著降低,LPS降低的总抗氧化能力、超氧化物歧化酶和还原型谷胱甘肽显著增加。发现LLE可通过上调空肠组织中[具体基因名称未给出]的mRNA和蛋白表达来减轻LPS诱导的氧化应激。总之,LLE通过调节[具体信号通路未给出]信号通路来减轻氧化应激、减少炎症因子并增加紧密连接蛋白的表达,从而减轻LPS诱导的肠道损伤。