Abstract: FR-PO964
Total Extracts of Single Chinese Medicine Herb Attenuates Renal Tubule Injury via Suppression of ERK1/2-Mediated NLRP3 Inflammasome Activation
Session Information
- Pathology and Lab Medicine: Basic
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1601 Pathology and Lab Medicine: Basic
Authors
- Li, Wei, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China
- Xia, Ping, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China
- Zhou, Yao, Xuzhou Medical University, Xuzhou, Jiangsu, China
- Sun, 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
Background
Abelmoschus Manihot (Linnaeus) Medik. is an herb used in traditional Chinese medicine to treat some kidney diseases. The chemical constituents in the plant are mainly flavonoids, organic acids, steroids and volatile compounds. Five flavonoids, hyperoside, myricetin, quercetin, isoquercitrin, and rutin, have been determined to be the major pharmacologically bioactive components via high-performance liquid chromatography (HPLC) that simultaneously quantifies the flavonoid compounds of Abelmoschus Manihot L. flower. To date, the detailed mechanisms by which Abelmoschus Manihot L. improves some kinds of renal disease are not fully understood. Our previous study showed that Abelmoschus Manihot L protects podocyte and reduce proteinuria in vivo.
Methods
In this study, we established Adriamycin-induced NRK-52E cells, the normal rat kidney epithelial cell line, and Sprague-Dawley rats with Adriamycin-induced nephropathy to evaluate the role and mechanisms of total extracts of Abelmoschus Manihot L. flower (TEA) on tubular cell both in vitro and in vivo.
Results
In Adriamycin-induced nephropathy rat model, TEA decreased proteinuria and attenuated renal tubule lesions. Interestingly, NLRP3 was increased mostly in tubule not in glomeruli and TEA inhibited the expression of NLRP3 in tubules. In vitro study, TEA ameliorated Adriamycin-induced cellular morphological changes, cell viability, and apoptosis through the suppression of protein oxidation and ERK1/2 signaling. However, this anti-oxidative stress role of TEA was independent of ROS inhibition. Adriamycin activated ERK1/2 signaling followed by activation of NLRP3 inflammasomes. TEA suppressed NLRP3 inflammasomes via inhibition of ERK1/2 signal transduction.
Conclusion
TEA protects renal tubular cells against toxity of Adriamycin via inhibition of ERK1/2-NLRP3 inflammasomes.
Funding
- Government Support - Non-U.S.