Dahuang Fuzi Decoction ameliorates tubular epithelial apoptosis and renal damage via inhibiting TGF-β1-JNK signaling pathway activation in vivo

Tu, Ya; Sun, Weijian; Wan, Yi‐Gang; Gao, Kun; Liu, Hong; Yu, Bing-Yin; Hu, Hao; Huang, Yanru

doi:10.1016/j.jep.2014.08.035

Cited by 44 publications

(33 citation statements)

References 35 publications

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“…More importantly, it has been proven to be effective. DFD, which is frequently used in TCM, has been shown to be effective in promoting diuresis, reducing proteinuria, and restoring renal function in patients with CKD [6]. Using the chronic AAN model, we demonstrated that oral administration of DFD at the dose of 5g/kg/d significantly decreased the levels of BUN, serum creatinine, and proteinuria and improved the histologic characteristics of renal fibrosis.…”

Section: Discussionmentioning

confidence: 90%

“…Dahuang Fuzi Decoction (DFD) is a traditional formula consisting of Da Huang (Radix et Rhizoma Rhei), Pao-fuZi (Radix Aconiti Lateralis Preparata), and Xi Xin (Radix et Rhizoma Asari) [6]. In clinics, DFD has been widely used to treat chronic dysentery, acute ileus, and CKD [7].…”

Section: Introductionmentioning

confidence: 99%

“…In clinics, DFD has been widely used to treat chronic dysentery, acute ileus, and CKD [7]. Most importantly, DFD has been shown to improve renal function significantly and the quality of life for CKD patients [6]. A high performance liquid chromatography-mass spectrometry (HPLC-MS) study found that three anthraquinones including rhein, aloe-emodin, and emodin are presented in rat plasma treated with DFD [7], suggesting that these compounds may improve renal function.…”

Section: Introductionmentioning

confidence: 99%

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Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

Shui

Sang

Yin

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Objectives. The effects of the traditional formula Dahuang Fuzi Decoction (DFD) on chronic aristolochic acid nephropathy (AAN) in mice and its underlying mechanisms were studied. Methods. Mice were randomly divided into the following six groups: the control group, the model group (AAN), the saline-treated group (AAN + vehicle), the normal dose DFD-treated group (AAN + NDFD), the high dose DFD-treated group (AAN + HDFD), and the rosiglitazone treated group (AAN + Rosi). After treating for 8 weeks, 24 h urine and blood samples were collected and the mice sacrificed to study the biochemical parameters associated with renal function. The samples were analyzed for renal fibrosis and mitochondrial dysfunction (MtD) markers. To achieve that, collagen III, collagen I, mitochondrial DNA copy numbers (mtDNA), mitochondrial membrane potential (MMP), ATP content, and ROS production were evaluated. Results. Our results showed that proteinuria, kidney function, and the renal pathological characteristics were improved by DFD and rosiglitazone. The expression of collagen III and collagen I decreased after treating with either DFD or rosiglitazone. Mitochondrial dysfunction based on the increase in ROS production, decrease in mitochondrial DNA copy numbers, and reduction of MMP and ATP content was improved by DFD and rosiglitazone. Conclusions. DFD could protect against renal impairments and ameliorate mitochondrial dysfunction in chronic AAN mice.

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

Shui

Sang

Yin

et al. 2017

Evidence-Based Complementary and Alternative Medicine

Self Cite

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“…There are two main apoptotic signaling pathways: the death receptor-mediated extrinsic pathway and the mitochondria-mediated intrinsic pathway 47 . The proteins of the Bcl-2 family are key regulators of the mitochondrial pathway, including pro-apoptotic members (such as Bax) and anti-apoptotic members (such as Bcl-2), which can regulate the activation of caspases that cleave a number of cellular proteins, such as caspase-3 47, 48 . Recent studies found that CRF rats had increased apoptosis levels, up-regulated Bax expression, and down-regulated Bcl-2 expression in renal tissues 48, 49 .…”

Section: Discussionmentioning

confidence: 99%

“…The proteins of the Bcl-2 family are key regulators of the mitochondrial pathway, including pro-apoptotic members (such as Bax) and anti-apoptotic members (such as Bcl-2), which can regulate the activation of caspases that cleave a number of cellular proteins, such as caspase-3 47, 48 . Recent studies found that CRF rats had increased apoptosis levels, up-regulated Bax expression, and down-regulated Bcl-2 expression in renal tissues 48, 49 . In line with the above findings, our results showed that the expression levels of Bax, Caspase-3, and Cleaved Caspase-3 were significantly increased and the expression level of Bcl-2 was dramatically decreased in CRF rats.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Luo

Wang

et al. 2017

Sci Rep

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Chronic renal failure (CRF) is a major public health problem worldwide. Hydrogen sulfide (H2S) plays important roles in renal physiological and pathophysiological processes. However, whether H2S could protect against CRF in rats remains unclear. In this study, we found that H2S alleviated gentamicin-induced nephrotoxicity by reducing reactive oxygen species (ROS)-mediated apoptosis in normal rat kidney-52E cells. We demonstrated that H2S significantly improved the kidney structure and function of CRF rats. We found that H2S decreased the protein levels of Bax, Caspase-3, and Cleaved-caspase-3, but increased the expression of Bcl-2. Treatment with H2S reduced the levels of malondialdehyde and ROS and increased the activities of superoxide dismutase and glutathione peroxidase. H2S significantly abolished the phosphorylation of extracellular signal-regulated protein kinase 1/2, c-Jun N-terminal kinase, and p38 in the kidney of CRF rats. Furthermore, H2S decreased the expression levels of tumor necrosis factor-α, interleukin (IL)-6, IL-10, and monocyte chemoattractant protein-1, as well as the protein levels of p50, p65, and p-p65 in the kidney of CRF rats. In conclusion, H2S could ameliorate adenine-induced CRF in rats by inhibiting apoptosis and inflammation through ROS/mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways.

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Mechanism of Rhubarb for Diabetic Kidney Disease through the AMPK/NF‐κB Signaling Pathway Based on Network Pharmacology

et al. 2022

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Rhubarb (Da‐huang in pinyin, Radix Rhei Et Rhizome in pharmaceutical name) is a heat‐clearing and laxative herbal medicine, which is widely used to treat diabetic kidney disease in China. The study aims to decrypt the underlying mechanisms of the treatment of diabetic kidney disease using a systems pharmacology approach. Active compounds and corresponding potential therapeutic targets were harvested by utilizing the database of TCMSP. DKD targets were adopted from DrugBank, OMIM, TTD, and GAD databases. Then a network of Rhubarb‐ compounds ‐ target ‐ DKD network was harvested. The PPI network was then generated by the String database and subjected to Cytoscape software to harvest major and core targets network by topological analysis. Genes from the core targets network were further subjected to GO and KEGG enrichment analysis to figure out potential targeting pathways. Human podocyte cells (HPC) were used to further investigate the mechanism of against DKD. A total of 6 active ingredients and 271 targets of Rhubarb were picked out. 11 cellular biological processes and 18 pathways of mostly associated with inflammatory response, apoptosis, fibrosis, and peripheral circulation. Moreover, experimental validation suggests that Rhubarb increased cell viability. Rhubarb extract significantly suppressed the expression of NF‐kappa B, Bcl‐2, Caspase‐3, and Cleaved Caspase‐3, promoted the expression of AMPK and Bax, and decreased the release of cytokines. Rhubarb could alleviate DKD via the molecular mechanisms predicted by network pharmacology.

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Dahuang Fuzi Decoction ameliorates tubular epithelial apoptosis and renal damage via inhibiting TGF-β1-JNK signaling pathway activation in vivo

Cited by 44 publications

References 35 publications

Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

Dahuang Fuzi Decoction Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in Chronic Aristolochic Acid Nephropathy

Hydrogen sulfide ameliorates chronic renal failure in rats by inhibiting apoptosis and inflammation through ROS/MAPK and NF-κB signaling pathways

Mechanism of Rhubarb for Diabetic Kidney Disease through the AMPK/NF‐κB Signaling Pathway Based on Network Pharmacology

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