title: Protective effects of Huang Qi Huai granules on adriamycin nephrosis in rats.
abstract: 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.
authors.affiliation: Department of Nephrology, Nanjing Children's Hospital, Nanjing Medical University, Nanjing, 210008, Jiangsu Province, China.
authors.forename: Chunhua
authors.initials: C
authors.lastname: Zhu
authors.forename: Songming
authors.initials: S
authors.lastname: Huang
authors.forename: Guixia
authors.initials: G
authors.lastname: Ding
authors.forename: Yanggang
authors.initials: Y
authors.lastname: Yuan
authors.forename: Qiuxia
authors.initials: Q
authors.lastname: Chen
authors.forename: Xiaoqin
authors.initials: X
authors.lastname: Pan
authors.forename: Ronghua
authors.initials: R
authors.lastname: Chen
authors.forename: Aihua
authors.initials: A
authors.lastname: Zhang
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D002461:Cell Line, Transformed; D019963:Clinical Chemistry Tests; D004195:Disease Models, Animal; D004317:Doxorubicin / Q000633:toxicity*; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D015870:Gene Expression / Q000187:drug effects; D053583:Interleukin-1beta / Q000097:blood; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000473:pathology; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D009401:Nephrosis / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D008517:Phytotherapy; D050199:Podocytes / Q000187:drug effects / Q000648:ultrastructure; D011507:Proteinuria / Q000175:diagnosis / Q000188:drug therapy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000903:Antibiotics, Antineoplastic; D004365:Drugs, Chinese Herbal; D053583:Interleukin-1beta; D047908:Intracellular Signaling Peptides and Proteins; C486607:Kirrel1 protein, rat; D008565:Membrane Proteins; C407223:NPHS2 protein; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D004317:Doxorubicin