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  • 标题:Shibi Tea ( Adinandra nitida) and Camellianin A Alleviate CCl 4-Induced Liver Injury in C57BL-6J Mice by Attenuation of Oxidative Stress, Inflammation, and Apoptosis
  • 本地全文:下载
  • 作者:Ruohong Chen ; Yingyi Lian ; Shuai Wen
  • 期刊名称:Nutrients
  • 电子版ISSN:2072-6643
  • 出版年度:2022
  • 卷号:14
  • 期号:15
  • DOI:10.3390/nu14153037
  • 语种:English
  • 出版社:MDPI Publishing
  • 摘要:Liver injury is a significant public health issue nowadays. Shibi tea is a non- Camellia tea prepared from the dried leaves of Adinandra nitida, one of the plants with the greatest flavonoid concentration, with Camellianin A (CA) being the major flavonoid. Shibi tea is extensively used in food and medicine and has been found to provide a variety of health advantages. The benefits of Shibi tea and CA in preventing liver injury have not yet been investigated. The aim of this study was to investigate the hepatoprotective effects of extract of Shibi tea (EST) and CA in mice with carbon tetrachloride (CCl 4)-induced acute liver injury. Two different concentrations of EST and CA were given to model mice by gavage for 3 days. Treatment with two concentrations of EST and CA reduced the CCl 4-induced elevation of the liver index, liver histopathological injury score, alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Western blotting and immunohistochemical analysis demonstrated that EST and CA regulated the oxidative stress signaling pathway protein levels of nuclear factor E2-related factor 2 (Nrf2)/heme-oxygenase-1 (HO-1), the expression of inflammatory cytokines, the phosphorylated nuclear factor-kappaB p65 (p-NF-κB)/nuclear factor-kappaB p65 (NF-κB) ratio, the phospho-p44/42 mitogen-activated protein kinase (p-MAPK), and the apoptosis-related protein levels of BCL2-associated X (Bax)/B cell leukemia/lymphoma 2 (Bcl2) in the liver. Taken together, EST and CA can protect against CCl 4-induced liver injury by exerting antioxidative stress, anti-inflammation, and anti-apoptosis.
  • 关键词:enAdinandra nitida(Theaceae)Camellianin Aliver injuryoxidative stressinflammationanti-apoptosis
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