Huang Qi Huai (HQH) granules, a mixture of Chinese herbs, contains trametes robiniophila murr, wolfberry fruit, and Polygonatum. We investigated the mechanism of the protective effects of HQH on adriamycin nephrosis (ADR) in rats. Adriamycin nephrotic rats were induced by a single dose of 5 mg/kg adriamycin. For the HQH-treated adriamycin nephrosis group, 1 day after treatment with 5 mg/kg adriamycin, the rats were administered once-daily oral gavage of 2 mg/kg HQH for 15 days. All the rats were killed at day 15. Histological changes were observed by light microscopy and transmission electron microscope. Nephrin and podocin expression levels were measured by real-time RT-PCR and Western blot. Proteinuria was measured by the Bradford protein assay. Serum TNF-α and IL-1β levels were evaluated by ELISA. Macrophage infiltration was detected by immunohistochemistry and immunoblotting, respectively. ADR rats showed heavy proteinuria, podocyte and tubulointerstitial injury, macrophage infiltration, and increased levels of serum cytokines TNF-α and IL-1β. HQH significantly ameliorated the adriamycin-induced renal injury. These data were validated in the cultured podocytes. The podocytes were treated by adriamycin in the presence or absence of HQH and nephrin and podocin expression and TNF-α and IL-1β synthesis and secretion were determined by real-time RT-PCR, immunoblotting, and ELISA, respectively. Adriamycin significantly reduced nephrin and podocin expression, which was significantly restored by the treatment of HQH. HQH treatment inhibited adriamycin-induced TNF-α and IL-1β expression. Our findings suggest that HQH significantly reduces proteinuria, prevents podocyte injury, and ameliorates tubulointerstitial damage. Inhibition of inflammatory cytokine expression and macrophage infiltration may be the protective mechanism of HQH.
This is a preview of subscription content, access via your institution.
Buy single article
Instant access to the full article PDF.
Tax calculation will be finalised during checkout.
Subscribe to journal
Immediate online access to all issues from 2019. Subscription will auto renew annually.
Tax calculation will be finalised during checkout.
Eddy AA, Symons JM (2003) Nephrotic syndrome in childhood. Lancet 362:629–639
Araya CE, Wasserfall CH, Brusko TM, Mu W, Segal MS, Johnson RJ, Garin EH (2006) A case of unfulfilled expectations. Cytokines in idiopathic minimal lesion nephrotic syndrome. Pediatr Nephrol 21:603–610
Huang Q (2004) Observation of curative effect on 62 cases of repeated respiratory tract infection of cerebral palsy by Huan Er Jin-Huai Ji Huang Ke Li. J Henan University Chin Med 19:65–65
Wang C (2007) Preventive and curative effect of Huan Erjin on children's repeated respiratory tract infection. China Pharmacist 10:1026–1027
Takahashi S, Wada N, Murakami H, Funaki S, Inagaki T, Harada K, Nagata M (2007) Triggers of relapse in steroid-dependent and frequently relapsing nephrotic syndrome. Pediatr Nephrol 22:232–236
Abeyagunawardena AS, Trompeter RS (2008) Increasing the dose of prednisolone during viral infections reduces the risk of relapse in nephrotic syndrome: a randomised controlled trial. Arch Dis Child 93:226–228
Turnberg D, Lewis M, Moss J, Xu Y, Botto M, Cook HT (2006) Complement activation contributes to both glomerular and tubulointerstitial damage in adriamycin nephropathy in mice. J Immunol 177:4094–4102
Wang SN, Hirschberg R (1999) Tubular epithelial cell activation and interstitial fibrosis. The role of glomerular ultrafiltration of growth factors in the nephrotic syndrome and diabetic nephropathy. Nephrol Dial Transplant 14:2072–2074
Marshall SM (2007) The podocyte: a potential therapeutic target in diabetic nephropathy? Curr Pharm Des 13:2713–2720
Sean Eardley K, Cockwell P (2005) Macrophages and progressive tubulointerstitial disease. Kidney Int 68:437–455
Khan SB, Cook HT, Bhangal G, Smith J, Tam FW, Pusey CD (2005) Antibody blockade of TNF-alpha reduces inflammation and scarring in experimental crescentic glomerulonephritis. Kidney Int 67:1812–1820
Takano Y, Yamauchi K, Hayakawa K, Hiramatsu N, Kasai A, Okamura M, Yokouchi M, Shitamura A, Yao J, Kitamura M (2007) Transcriptional suppression of nephrin in podocytes by macrophages: roles of inflammatory cytokines and involvement of the PI3K/Akt pathway. FEBS Lett 581:421–426
Tang WW, Feng L, Vannice JL, Wilson CB (1994) Interleukin-1 receptor antagonist ameliorates experimental anti-glomerular basement membrane antibody-associated glomerulonephritis. J Clin Invest 93:273–279
Bricio T, Molina A, Mampaso F (1992) Effect of anti-interleukin-1 administration to rats with adriamycin-induced nephrosis. APMIS 100:401–407
Le Hir M, Haas C, Marino M, Ryffel B (1998) Prevention of crescentic glomerulonephritis induced by anti-glomerular membrane antibody in tumor necrosis factor-deficient mice. Lab Invest 78:1625–1631
Wu Y, Dong J, Yuan L, Liang C, Ren K, Zhang W, Fang F, Shen J (2008) Nephrin and podocin loss is prevented by mycophenolate mofetil in early experimental diabetic nephropathy. Cytokine 44:85–91
Hess J, Angel P, Schorpp-Kistner M (2004) AP-1 subunits: quarrel and harmony among siblings. J Cell Sci 117:5965–5973
Karin M, Chang L (2001) AP-1–glucocorticoid receptor crosstalk taken to a higher level. J Endocrinol 169:447–451
This work was supported by grants from the National Natural Science Foundation of China (Nos. 30872803 and 30971376), the Natural Science Foundation of Jiangsu Province (No. BK2009046), and the Specialized Research Fund for the Doctoral Program of Higher Education of China (No. 20103234110006), State Education Ministry of China.
About this article
Cite this article
Zhu, C., Huang, S., Ding, G. et al. Protective effects of Huang Qi Huai granules on adriamycin nephrosis in rats. Pediatr Nephrol 26, 905–913 (2011). https://doi.org/10.1007/s00467-011-1808-y
- Nephrotic syndrome
- Huang Qi Huai