Paeoniflorin Prevents Diabetic Nephropathy in Rats

Department of Endocrinology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Comparative medicine (Impact Factor: 0.74). 12/2009; 59(6):557-66.
Source: PubMed


The aim of this study was to test the hypothesis that paeoniflorin prevents the progression of diabetic nephropathy by modulating the inflammatory process. Sprague-Dawley rats were divided into 5 groups: nondiabetic control rats; untreated diabetic model (DM) rats; and DM rats treated with 5, 10, or 20 mg/kg paeoniflorin in drinking water once daily. Rats received a single intravenous injection of streptozotocin to induce diabetes; 9 wk after injection, rats began the 8-wk daily paeoniflorin treatment regimen. Compared with that of nonDM controls, the urinary albumin:creatinine ratio was increased significantly in untreated DM rats; this ratio was decreased in DM rats treated with 5, 10, or 20 mg/kg paeoniflorin compared with that of untreated DM rats. In addition, paeoniflorin treatment effectively suppressed glomerular hypertrophy; blood glucose; the expression of transforming growth factor beta, type IV collagen, and intercellular adhesion molecule 1; and renal infiltration of macrophages compared with levels in untreated DM rats. Furthermore, renal nuclear factor kappaB activity was increased in untreated but not paeoniflorin-treated DM rats. In conclusion, our data suggest that the preventive effects of paeoniflorin may be mediated by its antiinflammatory actions.

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    ABSTRACT: The present study aims to explore the effects of paeoniflorin (PF), a monoterpene glycoside isolated from the roots of Paeonia lactiflora Pallas, on acute lung injury (ALI) and the possible mechanisms. ALI was induced in mice by an intratracheal instillation of lipopolysaccharide (LPS, 1 mg/kg), and PF was injected intraperitoneally 30 min prior to LPS administration. After 24 h, lung water content, histology, microvascular permeability and proinflammatory cytokines in the bronchoaveolar lavage fluid were evaluated. It was shown that PF (50, 100 mg/kg) could alleviate LPS-induced ALI, evidenced by reduced pulmonary edema, improved histological changes, and attenuated inflammatory cell accumulation in the interstitium and alveolar space as well as microvascular permeability. It also markedly down-regulated the expressions of proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α at both transcription and protein levels. Additionally, PF inhibited the phosphorylations of p38 MAP kinase (p38) and c-Jun NH2-terminal kinase (JNK) but not extracellular signal-regulated kinase (ERK), and prevented the activation of nuclear factor-kappa B (NF-κB) in the lung tissues. The findings suggest that PF is able to alleviate ALI, and the underlying mechanisms are probably attributed to decreasing the production of proinflammatory cytokines through down-regulation of the activation of p38, JNK and NF-κB pathways in lung tissues.
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    ABSTRACT: To investigate the effect of the Paeoniflorin (Pae), a main active component of total glucosides of paeony (TGP) extracted from the root of Paeonia lactiflora, on regulation of synoviocytes cultured from rats collagen-induced arthritis (CIA) in vitro. CIA was induced in male Sprague-Dawley rats immunized with chicken type II collagen (CCII) in Freund's complete adjuvant. The levels of interleukin-1 (IL-1), tumor necrosis factor α (TNF-α), prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP) were measured by radioimmunoassay. The proliferation responses was determined by the 3-(4,5-2dimethylthiazal-2yl) 2,5-diphenyltetrazoliumbromide (MTT) assay. Expression of E-prostanoid (EP(4)) receptor was detected by Western blotting technique. Treatment of Pae (2.5, 12.5, 62.5 μg/ml) significantly decreased the production of IL-1 and TNF-α. Recombinant interleukin-1 (rIL-1α) (10 ng/ml) apparently stimulated synoviocyte, thymocyte and splenocyte proliferation, and Pae (12.5, 62.5 μg/ml) inhibited abnormal proliferation responses stimulated by rIL-1α. Moreover, rIL-1α time- and concentration-dependently increased production of PGE(2). The production of PGE(2) produced by synoviocytes from CIA rats significantly inhibited by administration of Pae (12.5, 62.5 μg/ml). rIL-1α (10 ng/ml) decreased cAMP of synoviocytes cells treated for 24h. Similarly rIL-1α (0.1, 1, 10 ng/ml) induced a concentration-dependent decrease in the production of cAMP at 24h. Pae (12.5, 62.5 μg/ml) increased the production of cAMP in synoviocytes. The immunoblot, Pae (12.5, 62.5 μg/ml) apparently increased the expression of EP(4) receptor in synoviocytes stimulated by rIL-1α (10 ng/ml). The present study indicates that Pae might exert its anti-inflammatory effects through suppressing synoviocytes function and regulating immune cells responses in CIA rats, which might be associated with its ability to up-regulate the E-prostanoid (EP(4)) receptor protein expression and modulate intracellular cAMP level.
    No preview · Article · Aug 2011 · Journal of ethnopharmacology
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