2. Academic Validation
  3. Arachidonic Acid Metabolism and Kidney Inflammation

Arachidonic Acid Metabolism and Kidney Inflammation

  • Int J Mol Sci. 2019 Jul 27;20(15):3683. doi: 10.3390/ijms20153683.
Tianqi Wang 1 2,  Xianjun Fu 2 3,  Qingfa Chen 4,  Jayanta Kumar Patra 5,  Dongdong Wang 6 7,  Zhenguo Wang 8,  Zhibo Gai 9
Affiliations

Affiliations

  • 1 Traditional Chinese Medicine History and Literature, Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
  • 2 Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
  • 3 Key Laboratory of Traditional Chinese Medicine for Classical Theory, Ministry of Education, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
  • 4 The Institute for Tissue Engineering and Regenerative Medicine, The Liaocheng University, Liaocheng 252000, China.
  • 5 Research Institute of Biotechnology & Medical Converged Science, Dongguk University-Seoul, Goyangsi 10326, Korea.
  • 6 Institute of Clinical Chemistry, University Hospital Zurich, University of Zurich, Wagistrasse 14, 8952 Schlieren, Switzerland.
  • 7 Guizhou University of Traditional Chinese Medicine, Fei Shan Jie 32, Guiyang 550003, China.
  • 8 Institute for Literature and Culture of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, China. [email protected].
  • 9 Key Laboratory of Traditional Chinese Medicine for Classical Theory, Ministry of Education, Shandong University of Traditional Chinese Medicine, Jinan 250355, China. [email protected].
PMID: 31357612 DOI: 10.3390/ijms20153683
Abstract

As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), Lipoxygenase (LOX), and Cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by Cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 Enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.

Keywords

arachidonic acid; cyclooxygenase; cytochrome P450; kidney inflammation; lipoxygenase; therapeutic target.

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