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Abstract: TH-PO629

Rhein Attenuated Palmitic Acid-Induced Renal Tubular Cell Injury by Regulating AMPK-mTOR-Autophagy

Session Information

Category: Health Maintenance, Nutrition, and Metabolism

  • 1300 Health Maintenance, Nutrition, and Metabolism

Authors

  • Li, Wei, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, JIANGSU , China
  • Gao, Kun, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, JIANGSU , China
  • Xia, Ping, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, JIANGSU , China
  • Zhou, Yao, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, JIANGSU , China
  • Sun, Wei, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, JIANGSU , China

Group or Team Name

  • Division of Nephrology, Affiliated Hospital of Nanjing University of Chinese Medicine
Background

Rhubarb is one of the widely used Chinese medicine herbs in the treatment of some kidney diseases. Rhein is an important monomer composition of Rhubarb which has multiple biological effects. Our previous studies have found that Rhein suppressed autophagy to protect renal cells. However, the underlying mechanism is still unclear. Metabolism disorder, especially dyslipidemia, attracts more and more attentions in recent years. In current study, we evaluated the protective effects of Rhein and the underlying mechanisms in palmitic acid (PA)-induced cell injury.

Methods

To study the toxicity of lipid, we use different concentrations of PA to induce HK2, human proximal tubular cell, injury. CCK8 cell viability detection, Tunel staining, FITC/PI flow cytometry and western blot were employed to analyze the protective effects of Rhein in PA-triggered HK2 impairment. Western blot and Fluorescence microscope were used to evaluated autophagy. Oil O stanning and Bodipy Probe were used to detect lipid in the cell.

Results

PA induced HK2 cells detatchment from the bottom, morphological changes and loss of cell viability after 24h incubation. The Rhein obviously reduced the cell damage elicited by PA, improved morphological changes, attenuated the loss of cell viability. Western blot analysis indicated that Rhein inhibited PA-induced autophagy as evidenced by the change of LC3 I to LC3 II bands. In addition, the fluorescence optical microscopy observation showed that PA activated autophagy. Moreover, autophagy inhibitor, chloroquine, did not affect autophagy flow in western blot analysis. These reuslts indicated that PA did not influence lysome function. PA increased autophagy upstream by upregulating AMPK-mTOR possiblelly in western blot analysis. And the Rhein might prohibit AMPK to regulate mTOR - ULK1 pathway.

Conclusion

Rhein attenuated the PA-induced renal tubular cell injury by regulating AMPK-mTOR-Autophagy pathway.

Funding

  • Government Support - Non-U.S.