Baicalein protects renal tubular epithelial cells againsthypoxia-reoxygenation injury

Abstract

Background: 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).

Methods: Cultured human renal proximal tubular cell line HK-2 was exposed to 24 h of hypoxia (5% CO₂, 1% O₂, and 94% N₂), followed by 12 h of reoxygenation (5% CO₂, 21% O₂, and 74% N₂). 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.

Results: 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.

Conclusions: BAI protects renal tubular epithelial cells from HR injury by reducing inflammatory cytokine expression and oxidative stress.

Keywords:

• Baicalein
• oxidative stress
• inflammation
• hypoxia-reoxygenation
• renal tubular epithelial cell

Acknowledgments

We thank Bo-Zhi Cai for technical support and the Central Laboratory, The First Affiliated Hospital of Shantou University Medical College for providing facilities.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Youth Innovative Talents Project from the Educational Commission of Guangdong Province of China [2015KQNCX047] and Central Government Special Funds Supporting the Development of Local Colleges and Universities.