Keishibukuryogan Reduces Renal Injury in the Early Stage of Renal Failure in the Remnant Kidney Model

Nakagawa, Takako; Tashiro, Izumi; Fujimoto, Makoto; Jo, Michiko; Sakai, Shinya; Oka, Hiroshi; Goto, Hirozo; Shimada, Yutaka; Shibahara, Naotoshi

doi:10.1093/ecam/nep089

Cited by 10 publications

(12 citation statements)

References 37 publications

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“…We next evaluated the possible mechanism for the renoprotective effects observed in RK + SF rats. Previous studies documented the roles of several cytokines that are responsible for renal inflammation and fibrosis in RK model 23,24,31–33 . Therefore, we quantitative analyzed the gene expression of these cytokines in RK and RK + SF rats.…”

Section: Resultsmentioning

confidence: 99%

Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model

Nemoto

Kumagai

Ishizawa

et al. 2019

Sci Rep

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Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was significantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several different approaches confirmed the protective effects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal inflammation and fibrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were significantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcification is absent.

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Section: Resultsmentioning

confidence: 99%

Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model

Nemoto

Kumagai

Ishizawa

et al. 2019

Sci Rep

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“…Ninjinyoeito has also been reported to suppress cancer metastasis (16). On the other hand, Keishibukuryogan has been shown to suppress renal fibrosis, which is caused by TGF-β-induced EMT (17). Despite the inhibitory activity of CC extract, the possibility can not be excluded that other herbal medicines might play a role in concert with CC extract, because of the harmonization effects among various herbal medicines (11,12).…”

Section: Discussionmentioning

confidence: 99%

Procyanidin C1 from Cinnamomi Cortex inhibits TGF-β-induced epithelial-to-mesenchymal transition in the A549 lung cancer cell line

Kin

Kato

Kaneto

et al. 2013

International Journal of Oncology

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Abstract. Cancer metastasis is one of the most critical events in cancer patients, and the median overall survival of stage IIIb or IV patients with metastatic lung cancer in the TNM classification is only 8 or 5 months, respectively. We previously demonstrated that Juzentaihoto, a Japanese traditional medicine, can inhibit cancer metastasis through the activation of macrophages and T cells in mouse cancer metastatic models; however, the mechanism(s) through which Juzentaihoto directly affects tumor cells during the metastasis process and which herbal components from Juzentaihoto inhibit the metastatic potential have not been elucidated. In this study, we focused on the epithelial-to-mesenchymal transition (EMT), which plays an important role in the formation of cancer metastasis. We newly determined that only the Cinnamomi Cortex (CC) extract, one of 10 herbal components of Juzentaihoto, inhibits TGF-β-induced EMT. Moreover, the contents of catechin trimer in CC extracts were significantly correlated with the efficacy of inhibiting TGF-β-induced EMT. Finally, the structure of the catechin trimer from CC extract was chemically identified as procyanidin C1 and the compound showed inhibitory activity against TGF-β-induced EMT. This illustrates that procyanidin C1 is the main active compound in the CC extract responsible for EMT inhibition and that procyanidin C1 could be useful as a lead compound to develop inhibitors of cancer metastasis and other diseases related to EMT.

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“…by ablation of approximately 2/3 of the left kidney and then removal of the right kidney by ligation of renal artery, vein, and ureter ten days later. As an adaptive response to the renal ablation, the remnant kidney underwent hypertrophy, resulting in proteinuria, azotemia, and renal fibrosis with glomerular sclerosis and tubulointerstitial scarring over time [ 7 ].…”

Section: Methodsmentioning

confidence: 99%

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

Han

Chen

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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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 PPARγ, 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, PPARγ, OPN, fibronectin, and laminins and is useful for therapy of CRF.

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Keishibukuryogan Reduces Renal Injury in the Early Stage of Renal Failure in the Remnant Kidney Model

Cited by 10 publications

References 37 publications

Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model

Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model

Procyanidin C1 from Cinnamomi Cortex inhibits TGF-β-induced epithelial-to-mesenchymal transition in the A549 lung cancer cell line

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

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