Abstract
Abelmoschus manihot (L.) Medik. (Malvaceae) is a herb used in traditional Chinese medicine to treat some kidney diseases. To date, the detailed mechanisms by which A. manihot improves some kinds of renal disease are not fully understood. In this study, we established Adriamycin-induced NRK-52E cells, the normal rat kidney epithelial cell line, injury, and Sprague-Dawley rats with Adriamycin-induced nephropathy to evaluate the role and mechanisms of total extracts of A. manihot flower (TEA) both in vitro and in vivo. We found that 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; decreased proteinuria and attenuated renal tubule lesions; and inhibited the expression of NLRP3 in tubules in rats with Adriamycin nephropathy. Collectively, TEA protects renal tubular cells against Adriamycin-induced tubule injury via inhibition of ROS-ERK1/2-NLRP3 inflammasomes.
Highlights
Renal tubular cells constitute most of the mass of the kidney and maintain normal renal structure and function
We demonstrated that TEA attenuated Adriamycin-induced renal tubular cell injury
This protective role of TEA is ascribed to the inhibition of reactive oxygen species (ROS)-extracellular-signal–regulated kinases 1 and 2 (ERK1/2)-NLRP3 inflammasome activation (Figure 10)
Summary
Renal tubular cells constitute most of the mass of the kidney and maintain normal renal structure and function. Tubular lesions and recovery play crucial roles in epithelial-to-mesenchymal transition, renal fibrosis, acute kidney injury to chronic kidney. The extent of renal dysfunction is closely associated with changes in glomerular and tubulointerstitial injury. As a final common pathway, tubular injury is a major determinant in the progression of kidney disease (Nath, 1992). It is clinically significant to fully understand the tubule and preservation of the structure and function of renal tubular epithelial cells may provide a novel therapy for slowing the progression of kidney disease. To date, efforts aimed at the preservation of renal tubular cells via pharmacological interventions have not yet achieved clinical significance. Herbs associated with traditional Chinese medicine are perceived to be a cost-efficient alternative
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