a Department of Traditional Chinese Medicine , The First Affiliated Hospital of Shantou University Medical College , Shantou , China.
b Department of Nephrology , The First Affiliated Hospital of Shantou University Medical College , Shantou , China.
Ren Fail. 2018 Nov;40(1):603-610. doi: 10.1080/0886022X.2018.1532910.
To investigate the protective effects and mechanism of baicalein (BAI), a naturally occurring flavonoid, against hypoxia-reoxygenation (HR) injury in renal tubular epithelial cells (HK-2).
Cultured human renal proximal tubular cell line HK-2 was exposed to 24 h of hypoxia (5% CO, 1% O, and 94% N), followed by 12 h of reoxygenation (5% CO, 21% O, and 74% N). HK-2 cells were divided into three groups: control, HR, and HR-BAI (0.3 µg/ml). Reactive oxygen species (ROS) were measured and cell apoptosis was analyzed by flow cytometry and morphology. ELISAs were performed to determine the levels of IL-1, intercellular adhesion molecule-1 (ICAM-1), and monocyte chemotactic protein-1 (MCP-1). IL-1β, ICAM-1, and MCP-1 mRNA levels were determined by real-time quantitative PCR.
HK-2 cells that underwent HR exhibited increases in IL-1β expression by 0.94%, ROS by 0.59%, ICAM-1 expression by 0.8%, and MCP-1 expression by 1.2%. Moreover, HK-2 cell apoptosis was increased after HR (p < .05). Compared with the HR group, BAI treatment reduced the elevation of oxidative stress (ROS) by 0.76%, as well as HR-mediated induction of IL-1β and apoptosis of HK2 cells. Protein and mRNA levels of ICAM-1 and MCP-1 were also reduced.
BAI protects renal tubular epithelial cells from HR injury by reducing inflammatory cytokine expression and oxidative stress.
研究目的在于探讨黄芩素（BAI）这种天然黄酮类化合物对肾小管上皮细胞（HK-2）缺氧再复氧（HR）损伤的保护作用及其机制。
将培养的人近端肾小管细胞系 HK-2 置于 24 h 低氧（5% CO、1% O 和 94% N）环境中，随后进行 12 h 的复氧（5% CO、21% O 和 74% N）处理。将 HK-2 细胞分为三组：对照组、HR 组和 HR-BAI（0.3 µg/ml）组。通过流式细胞术和形态学分析检测活性氧（ROS），并分析细胞凋亡。采用 ELISA 法测定白细胞介素-1（IL-1）、细胞间黏附分子-1（ICAM-1）和单核细胞趋化蛋白-1（MCP-1）的水平。采用实时定量 PCR 法测定 IL-1β、ICAM-1 和 MCP-1 的 mRNA 水平。
HR 组 HK-2 细胞的 IL-1β 表达增加了 0.94%，ROS 增加了 0.59%，ICAM-1 表达增加了 0.8%，MCP-1 表达增加了 1.2%。此外，HR 后 HK-2 细胞凋亡增加（p <.05）。与 HR 组相比，BAI 处理降低了氧化应激（ROS）的升高（降低了 0.76%），以及 HR 介导的 HK2 细胞中 IL-1β 的诱导和凋亡。ICAM-1 和 MCP-1 的蛋白和 mRNA 水平也降低。
BAI 通过降低炎症细胞因子表达和氧化应激，保护肾小管上皮细胞免受 HR 损伤。
