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      Protective Effects of Bu-Shen-Huo-Xue Formula against 5/6 Nephrectomy-Induced Chronic Renal Failure in Rats

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          Abstract

          Chronic renal failure (CRF) is a serious disease related to increasing incidence and prevalence as well as decline in quality of life. Bu-Shen-Huo-Xue formula (BSHX), one of traditional herbal formulations, has been clinically employed to treat CRF for decades, but the mechanisms involved have not been investigated. In the present study, we investigated the effects of BSHX on some closely related parameters in 5/6 nephrectomy CRF rats. Rats with CRF were divided into five groups, namely, one control group, one enalapril group, and three BSHX treatment groups (0.25, 0.5, and 1 g/kg·d). The rats subjected to sham operation were used as a normal control. After eight weeks of treatment, BSHX significantly decreased the levels of Scr and BUN, downregulated the mRNA expression levels of TGF- β 1, CTGF, NF- κB, TNF- α, and OPN, upregulated the mRNA expression of PPAR γ, and reduced in situ expression of fibronectin and laminins. Histological findings also showed significant amelioration of the damaged renal tissue. BSHX protects 5/6 nephrectomy rats against chronic renal failure probably via regulating the expression of TNF- α, NF- κB, TGF- β 1, CTGF, PPAR γ, OPN, fibronectin, and laminins and is useful for therapy of CRF.

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          Inflamed adipose tissue: a culprit underlying the metabolic syndrome and atherosclerosis.

          Birgit Gustafson, Ann Hammarstedt, Christian Andersson … (2007)
          The metabolic syndrome is associated with a dysregulated adipose tissue; in part a consequence of adipose cell enlargement and the associated infiltration of macrophages. Adipose cell enlargement leads to a proinflammatory state in the cells with reduced secretion of adiponectin and with increased secretion of several cytokines and chemokines including interleukin (IL)-6, IL-8, and MCP-1. MCP-1 has been shown to play an important role for the associated recruitment of macrophages into the adipose tissue. The increased release of cytokines leads to an impaired differentiation of the preadipocytes with reduced lipid accumulation and induction of adiponectin, thus promoting ectopic lipid storage. In particular tumor necrosis factor (TNF) alpha, but also IL-6, has been shown to induce these effects in preadipocytes and this is associated with an increased Wnt signaling maintaining the cells in an undifferentiated and proinflammatory state. The proinflammatory state in the adipose tissue also leads to a local insulin resistance including an impaired inhibitory effect of insulin on FFA release. The insulin resistance further supports the proinflammatory state because insulin, by itself, is both antilipolytic and antiinflammatory by antagonizing cytokine-induced activation of STAT signaling.
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            Peroxisome proliferator-activated receptors (PPARs): novel therapeutic targets in renal disease.

            Richard M. Breyer, Youfei Guan (2001)
            Peroxisome proliferator-activated receptors (PPARs): Novel therapeutic targets in renal disease. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-dependent transcription factors. PPARs play an important role in the general transcriptional control of numerous cellular processes, including lipid metabolism, glucose homeostasis, cell cycle progression, cell differentiation, inflammation and extracellular matrix remodeling. Three PPAR isoforms, designated PPARalpha, PPARbeta and PPARgamma, have been cloned and are differentially expressed in several tissues including the kidney. PPARalpha primary regulates lipid metabolism and modulates inflammation. PPARalpha is the molecular target of the hypolipidemic fibrates including bezafibrate and clofibrate. PPARbeta participates in embryonic development, implantation and bone formation. PPARgamma is a key factor in adipogenesis and also plays an important role in insulin sensitivity, cell cycle regulation and cell differentiation. Antidiabetic thiazolidinediones (TZDs) such as troglitazone and rosiglitazone are specific ligands of PPARgamma, and this interaction is responsible for the insulin-sensitizing and hypoglycemic effect of these drugs. The kidney has been shown to differentially express all PPAR isoforms. PPARalpha is predominantly expressed in proximal tubules and medullary thick ascending limbs, while PPARgamma is expressed in medullary collecting ducts, pelvic urothelium and glomerular mesangial cells. PPARbeta is ubiquitously expressed at low levels in all segments of nephron. Accumulating data has begun to emerge suggesting physiological and pathophysiological roles of PPARs in several tissues including the kidney. The availability of PPAR-selective agonists and antagonists may provide a new approach to modulate the renal response to diseases including glomerulonephritis, glomerulosclerosis and diabetic nephropathy.
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              New model for adenine-induced chronic renal failure in mice, and the effect of gum acacia treatment thereon: comparison with rats.

              Badreldin Ali, Suhail Al-Salam, Mohammed Al Za'abi … (2016)
              This study aimed at comparing the effects of feeding mice and rats with adenine to induce a state of chronic renal failure (CRF), and to assess the effect of treatment with gum acacia (GA) thereon. We compared the outcome, in mice, of feeding adenine at three different doses (0.75%, 0.3%, and 0.2%, w/w). Biochemical and histopathological studies were conducted in plasma, urine and renal homogenates from both species. When mice and rats were fed adenine (0.75%, w/w), all treated rats survived the treatment, but all treated mice died within 1-2 days. The dosage in mice was reduced to 0.3%, w/w, for 4 weeks, but again all treated mice died within 3-4 days. A further reduction in the dosage in mice to 0.2%, w/w, for 4 weeks resulted in no mortality, and produced alterations similar to those observed in rats fed adenine at a dose of 0.75%,w/w, for 4 weeks. Plasma creatinine, urea and urinary protein were significantly increased (P<0.001) in adenine-treated mice and rats, and this action was incompletely, but significantly (P<0.05), reversed by GA. Adenine significantly (P<0.001) reduced superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentration in renal homogenates from both species, and these reductions were significantly (P<0.05) ameliorated by GA. Our data suggest that mice are more sensitive to adenine than rats, and that a dose of adenine of 0.2%, w/w, for 4 weeks in mice is suggested as a model for CRF. In both models, GA (15%, w/v, in the drinking water for 4 weeks) given concomitantly with adenine ameliorated the severity of CRF to a similar extent. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Evid Based Complement Alternat Med
                Journal ID (iso-abbrev): Evid Based Complement Alternat Med
                Journal ID (publisher-id): ECAM
                Title: Evidence-based Complementary and Alternative Medicine : eCAM
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1741-427X
                ISSN (Electronic): 1741-4288
                Publication date (Print): 2014
                Publication date (Electronic): 29 April 2014
                Publication date PMC-release: 29 April 2014
                Volume: 2014
                Electronic Location Identifier: 589846
                Affiliations
                1Division of Nephrology, Shanghai Seventh People's Hospital, Shanghai 200137, China
                2School of Traditional Chinese Medicine, Capital Medical University, Beijing 100069, China
                Author notes

                Academic Editor: Yong Chool Boo

                Article
                DOI: 10.1155/2014/589846
                PMC ID: 4020566
                PubMed ID: 24864155
                SO-VID: 4e68cee7-1beb-43fa-9291-0184ba40a836
                Copyright © Copyright © 2014 Jian-Rao Lu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 December 2013
                Date revision received : 20 February 2014
                Date accepted : 10 March 2014
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Complementary & Alternative medicine
                Data availability:
                ScienceOpen disciplines: Complementary & Alternative medicine

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