Modified Huangqi Chifeng decoction (MHCD) has been used to reduce proteinuria in immunoglobulin A nephropathy (IgAN) for many years. Previously, we have demonstrated its protective role in glomerular mesangial cells. Podocyte injury, another key factor associated with proteinuria in IgAN, has also attracted increasing attention. However, whether MHCD can reduce proteinuria by protecting podocytes remains unclear. The present study aimed to investigate the protective effects of MHCD against podocyte injury in a rat model of IgAN. To establish the IgAN model, rats were administered bovine serum albumin, carbon tetrachloride, and lipopolysaccharide. MHCD in three doses or telmisartan was administered once daily for 8 weeks ( = 10 rats/group). Rats with IgAN developed proteinuria at week 6, which worsened over time until drug intervention. After drug intervention, MHCD reduced proteinuria and had no effect on liver and kidney function. Furthermore, MHCD alleviated renal pathological lesions, hyperplasia of mesangial cells, mesangial matrix expansion, and podocyte foot process fusion. Western blot analysis revealed that MHCD increased the expression of the podocyte-associated proteins nephrin and podocalyxin. Additionally, we stained podocyte nuclei with an antibody for Wilms' tumor protein one and found that MHCD increased the podocyte number in rats with IgAN. In conclusion, these results demonstrate that MHCD attenuates proteinuria by reducing podocyte injury.
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http://dx.doi.org/10.3389/fphar.2021.714584 | DOI Listing |
Sci Rep
January 2025
The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, People's Republic of China.
Chronic kidney disease (CKD) stands as a formidable global health challenge, often advancing to end-stage renal disease (ESRD) with devastating morbidity and mortality. At the central of this progression lies podocyte injury, a critical determinant of glomerular dysfunction. Compound K (CK), a bioactive metabolite derived from ginsenoside, has emerged as a compelling candidate for nephroprotective therapy.
View Article and Find Full Text PDFNat Commun
January 2025
Vertex Pharmaceuticals Incorporated, Boston, MA, USA.
Chronic kidney disease affects ~10% of people worldwide and there are no disease modifying therapeutics that address the underlying cause of any form of kidney disease. Genome wide association studies have identified the G1 and G2 variants in the apolipoprotein L1 (APOL1) gene as major contributors to a subtype of proteinuric kidney disease now referred to as APOL1-mediated kidney disease (AMKD). We hypothesized that inhibition of APOL1 could have therapeutic potential for this genetically-defined form of kidney disease.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Renal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Background: Particulate matter (PM2.5) has been implicated in the development of membranous nephropathy (MN), but the underlying mechanism has yet to be fully understood. Oxidative stress is an essential factor of PM2.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Department of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China. Electronic address:
Adv Sci (Weinh)
December 2024
Department of Kidney Research Institute, Seoul National University Medical Research Center, Seoul, South Korea.
Podocyte injury and proteinuria in glomerular disease are critical indicators of acute kidney injury progression to chronic kidney disease. Renal mitochondrial dysfunction, mediated by intracellular calcium levels and oxidative stress, is a major contributor to podocyte complications. Despite various strategies targeting mitochondria to improve kidney function, effective treatments remain lacking.
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